Samstag, Juli 30, 2022
StartBiochemistrySkeletal and extraskeletal issues of biomineralization

Skeletal and extraskeletal issues of biomineralization


  • Arnold, A. et al. Hormonal regulation of biomineralization. Nat. Rev. Endocrinol. 17, 261–275 (2021).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Hasegawa, T. Ultrastructure and organic perform of matrix vesicles in bone mineralization. Histochem. Cell Biol. 149, 289–304 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Azoidis, I., Cox, S. C. & Davies, O. G. The function of extracellular vesicles in biomineralisation: present perspective and software in regenerative drugs. J. Tissue Eng. 9, 2041731418810130 (2018).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Golub, E. E. Function of matrix vesicles in biomineralization. Biochim. Biophys. Acta 1790, 1592–1598 (2009).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Orimo, H. The mechanism of mineralization and the function of alkaline phosphatase in well being and illness. J. Nippon Med. Sch. 77, 4–12 (2010).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Ali, S. Y., Sajdera, S. W. & Anderson, H. C. Isolation and characterization of calcifying matrix vesicles from epiphyseal cartilage. Proc. Natl Acad. Sci. USA 67, 1513–1520 (1970).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Morris, D. C., Masuhara, Ok., Takaoka, Ok., Ono, Ok. & Anderson, H. C. Immunolocalization of alkaline phosphatase in osteoblasts and matrix vesicles of human fetal bone. Bone Min. 19, 287–298 (1992).

    CAS 
    Article 

    Google Scholar
     

  • Anderson, H. C. The function of matrix vesicles in physiological and pathological calcification. Curr. Opin. Orthop. 18, 428–433 (2007).

    Article 

    Google Scholar
     

  • Anderson, H. C. Molecular biology of matrix vesicles. Clin. Orthop. Relat. Res. 314, 266–280 (1995).


    Google Scholar
     

  • Asmussen, N., Lin, Z., McClure, M. J., Schwartz, Z. & Boyan, B. D. Regulation of extracellular matrix vesicles through fast responses to steroid hormones throughout endochondral bone formation. Steroids 142, 43–47 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shapiro, I. M., Landis, W. J. & Risbud, M. V. Matrix vesicles: are they anchored exosomes? Bone 79, 29–36 (2015).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Masaoutis, C. & Theocharis, S. The function of exosomes in bone reworking: implications for bone physiology and illness. Dis. Markers 2019, 9417914 (2019).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Bonucci, E. Bone mineralization. Entrance. Biosci. 17, 100–128 (2012).

    CAS 
    Article 

    Google Scholar
     

  • Balcerzak, M. et al. The roles of annexins and alkaline phosphatase in mineralization course of. Acta Biochim. Pol. 50, 1019–1038 (2003).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Kirsch, T., Harrison, G., Golub, E. E. & Nah, H. D. The roles of annexins and kinds II and X collagen in matrix vesicle-mediated mineralization of progress plate cartilage. J. Biol. Chem. 275, 35577–35583 (2000).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Guicheux, J. et al. A novel in vitro tradition system for evaluation of purposeful function of phosphate transport in endochondral ossification. Bone 27, 69–74 (2000).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Yoshiko, Y., Candeliere, G. A., Maeda, N. & Aubin, J. E. Osteoblast autonomous Pi regulation through Pit1 performs a task in bone mineralization. Mol. Cell Biol. 27, 4465–4474 (2007).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Millan, J. L. The function of phosphatases within the initiation of skeletal mineralization. Calcif. Tissue Int. 93, 299–306 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Addison, W. N., Azari, F., Sorensen, E. S., Kaartinen, M. T. & McKee, M. D. Pyrophosphate inhibits mineralization of osteoblast cultures by binding to mineral, up-regulating osteopontin, and inhibiting alkaline phosphatase exercise. J. Biol. Chem. 282, 15872–15883 (2007).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Terkeltaub, R. A. Inorganic pyrophosphate technology and disposition in pathophysiology. Am. J. Physiol. Cell Physiol. 281, C1–C11 (2001).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Brylka, L. & Jahnen-Dechent, W. The function of fetuin-A in physiological and pathological mineralization. Calcif. Tissue Int. 93, 355–364 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Zoch, M. L., Clemens, T. L. & Riddle, R. C. New insights into the biology of osteocalcin. Bone 82, 42–49 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Grynpas, M. D., Chachra, D. & Limeback, H. in The Osteoporosis Primer Vol. 23 318-330 (Cambridge College Press, 2000).

  • Boivin, G., Chavassieux, P., Chapuy, M. C., Baud, C. A. & Meunier, P. J. Skeletal fluorosis: histomorphometric evaluation of bone modifications and bone fluoride content material in 29 sufferers. Bone 10, 89–99 (1989).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Grynpas, M. D. Fluoride results on bone crystals. J. Bone Min. Res. 5 (Suppl. 1), S169–S175 (1990).

    CAS 

    Google Scholar
     

  • Moreno, E. C., Kresak, M. & Zahradnik, R. T. Physicochemical points of fluoride-apatite programs related to the examine of dental caries. Caries Res. 11 (Suppl. 1), 142–171 (1977).

    PubMed 
    Article 

    Google Scholar
     

  • Grynpas, M. D., Patterson-Allen, P. & Simmons, D. J. The modifications in high quality of mandibular bone mineral in in any other case completely immobilized rhesus monkeys. Calcif. Tissue Int. 39, 57–62 (1986).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Chavassieux, P., Seeman, E. & Delmas, P. D. Insights into materials and structural foundation of bone fragility from illnesses related to fractures: how determinants of the biomechanical properties of bone are compromised by illness. Endocr. Rev. 28, 151–164 (2007).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Whyte, M. P. Hypophosphatasia-aetiology, nosology, pathogenesis, analysis and therapy. Nat. Rev. Endocrinol. 12, 233–246 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Weiss, M. J. et al. A missense mutation within the human liver/bone/kidney alkaline phosphatase gene inflicting a deadly type of hypophosphatasia. Proc. Natl Acad. Sci. USA 85, 7666–7669 (1988).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Weiss, M. J. et al. Construction of the human liver/bone/kidney alkaline phosphatase gene. J. Biol. Chem. 263, 12002–12010 (1988).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Millan, J. L. & Whyte, M. P. Alkaline phosphatase and hypophosphatasia. Calcif. Tissue Int. 98, 398–416 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Whyte, M. P. Hypophosphatasia: enzyme alternative remedy brings new alternatives and new challenges. J. Bone Min. Res. 32, 667–675 (2017).

    CAS 
    Article 

    Google Scholar
     

  • Whyte, M. P. et al. Asfotase alfa remedy for youngsters with hypophosphatasia. JCI Perception 1, e85971 (2016).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Whyte, M. P., McAlister, W. H., Mumm, S. & Bierhals, A. J. No vascular calcification on cardiac computed tomography spanning asfotase alfa therapy for an aged lady with hypophosphatasia. Bone 122, 231–236 (2019).

    PubMed 
    Article 

    Google Scholar
     

  • Whyte, M. P. et al. Asfotase alfa for infants and younger youngsters with hypophosphatasia: 7 yr outcomes of a single-arm, open-label, section 2 extension trial. Lancet Diabetes Endocrinol. 7, 93–105 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mornet, E. Hypophosphatasia: the mutations within the tissue-nonspecific alkaline phosphatase gene. Hum. Mutat. 15, 309–315 (2020).

    Article 

    Google Scholar
     

  • Whyte, M. P. et al. Hypophosphatasia: validation and enlargement of the medical nosology for youngsters from 25 years expertise with 173 pediatric sufferers. Bone 75, 229–239 (2015).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Whyte, M. P. et al. Enzyme-replacement remedy in life-threatening hypophosphatasia. N. Engl. J. Med. 366, 904–913 (2012).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Guanabens, N. et al. Calcific periarthritis as the one medical manifestation of hypophosphatasia in middle-aged sisters. J. Bone Min. Res. 29, 929–934 (2014).

    CAS 
    Article 

    Google Scholar
     

  • Camacho, P. M. et al. Grownup hypophosphatasia handled with teriparatide: report of two sufferers and overview of the literature. Endocr. Pract. 22, 941–950 (2016).

    PubMed 
    Article 

    Google Scholar
     

  • Sutton, R. A., Mumm, S., Coburn, S. P., Ericson, Ok. L. & Whyte, M. P. “Atypical femoral fractures” throughout bisphosphonate publicity in grownup hypophosphatasia. J. Bone Min. Res. 27, 987–994 (2012).

    CAS 
    Article 

    Google Scholar
     

  • Sobel, E. H., Clark, L. C. Jr, Fox, R. P. & Robinow, M. Rickets, deficiency of alkaline phosphatase exercise and untimely lack of tooth in childhood. Pediatrics 11, 309–322 (1953).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Ornoy, A., Adomian, G. E. & Rimoin, D. L. Histologic and ultrastructural research on the mineralization course of in hypophosphatasia. Am. J. Med. Genet. 22, 743–758 (1985).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Anderson, H. C., Hsu, H. H., Morris, D. C., Fedde, Ok. N. & Whyte, M. P. Matrix vesicles in osteomalacic hypophosphatasia bone include apatite-like mineral crystals. Am. J. Pathol. 151, 1555–1561 (1997).

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • McKenna, M. J., Martin-Grace, J., Crowley, R., Twomey, P. J. & Kilbane, M. T. Congenital hypophosphataemia in adults: determinants of bone turnover markers and amelioration of renal phosphate losing following whole parathyroidectomy. J. Bone Min. Metab. 37, 685–693 (2019).

    CAS 
    Article 

    Google Scholar
     

  • Haffner, D. et al. Medical follow suggestions for the analysis and administration of X-linked hypophosphataemia. Nat. Rev. Nephrol. 15, 435–455 (2019).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Marcucci, G. et al. Phosphate losing issues in adults. Osteoporos. Int. 29, 2369–2387 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Manghat, P., Sodi, R. & Swaminathan, R. Phosphate homeostasis and issues. Ann. Clin. Biochem. 51, 631–656 (2014).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shimada, T. et al. Focused ablation of Fgf23 demonstrates a vital physiological function of FGF23 in phosphate and vitamin D metabolism. J. Clin. Make investments. 113, 561–568 (2004).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Goretti Penido, M. & Alon, U. S. Phosphate homeostasis and its function in bone well being. Pediatr. Nephrol. 27, 2039–2048 (2012).

    PubMed 
    Article 

    Google Scholar
     

  • Tiosano, D. & Hochberg, Z. Hypophosphatemia: the frequent denominator of all rickets. J. Bone Min. Metab. 27, 392–401 (2009).

    Article 

    Google Scholar
     

  • Beck-Nielsen, S. S. et al. FGF23 and its function in X-linked hypophosphatemia-related morbidity. Orphanet J. Uncommon Dis. 14, 58 (2019).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Bai, X. et al. CYP24 inhibition as a therapeutic goal in FGF23-mediated renal phosphate losing issues. J. Clin. Make investments. 126, 667–680 (2016).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Beck-Nielsen, S. S., Brock-Jacobsen, B., Gram, J., Brixen, Ok. & Jensen, T. Ok. Incidence and prevalence of dietary and hereditary rickets in southern Denmark. Eur. J. Endocrinol. 160, 491–497 (2009).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Liu, S., Guo, R. & Quarles, L. D. Cloning and characterization of the proximal murine Phex promoter. Endocrinology 142, 3987–3995 (2001).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Weng, C. et al. A de novo mosaic mutation of PHEX in a boy with hypophosphatemic rickets. J. Hum. Genet. 61, 223–227 (2016).

    PubMed 
    Article 

    Google Scholar
     

  • Whyte, M. P., Schranck, F. W. & Armamento-Villareal, R. X-linked hypophosphatemia: a seek for gender, race, anticipation, or dad or mum of origin results on illness expression in youngsters. J. Clin. Endocrinol. Metab. 81, 4075–4080 (1996).

    CAS 
    PubMed 

    Google Scholar
     

  • Linglart, A. et al. Therapeutic administration of hypophosphatemic rickets from infancy to maturity. Endocr. Join. 3, R13–R30 (2014).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Alon, U. S. et al. Hypertension in hypophosphatemic rickets — function of secondary hyperparathyroidism. Pediatr. Nephrol. 18, 155–158 (2003).

    PubMed 
    Article 

    Google Scholar
     

  • Barros, N. M. et al. Proteolytic processing of osteopontin by PHEX and accumulation of osteopontin fragments in Hyp mouse bone, the murine mannequin of X-linked hypophosphatemia. J. Bone Min. Res. 28, 688–699 (2013).

    CAS 
    Article 

    Google Scholar
     

  • Addison, W. N., Masica, D. L., Grey, J. J. & McKee, M. D. Phosphorylation-dependent inhibition of mineralization by osteopontin ASARM peptides is regulated by PHEX cleavage. J. Bone Min. Res. 25, 695–705 (2010).

    CAS 
    Article 

    Google Scholar
     

  • Murthy, A. S. X-linked hypophosphatemic rickets and craniosynostosis. J. Craniofac Surg. 20, 439–442 (2009).

    PubMed 
    Article 

    Google Scholar
     

  • Zivicnjak, M. et al. Age-related stature and linear physique segments in youngsters with X-linked hypophosphatemic rickets. Pediatr. Nephrol. 26, 223–231 (2011).

    PubMed 
    Article 

    Google Scholar
     

  • Carpenter, T. O., Imel, E. A., Holm, I. A., Jan de Beur, S. M. & Insogna, Ok. L. A clinician’s information to X-linked hypophosphatemia. J. Bone Min. Res. 26, 1381–1388 (2011).

    Article 

    Google Scholar
     

  • Balsan, S. & Tieder, M. Linear progress in sufferers with hypophosphatemic vitamin D-resistant rickets: affect of therapy routine and parental top. J. Pediatr. 116, 365–371 (1990).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Chaussain-Miller, C. et al. Dental abnormalities in sufferers with familial hypophosphatemic vitamin D-resistant rickets: prevention by early therapy with 1-hydroxyvitamin D. J. Pediatr. 142, 324–331 (2003).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Biosse Duplan, M. et al. Phosphate and vitamin D forestall periodontitis in X-linked hypophosphatemia. J. Dent. Res. 96, 388–395 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Boukpessi, T. et al. Osteopontin and the dento-osseous pathobiology of X-linked hypophosphatemia. Bone 95, 151–161 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Che, H. et al. Impaired high quality of life in adults with X-linked hypophosphatemia and skeletal signs. Eur. J. Endocrinol. 174, 325–333 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Faraji-Bellee, C. A. et al. Growth of enthesopathies and joint structural harm in a murine mannequin of X-linked hypophosphatemia. Entrance. Cell Dev. Biol. 8, 854 (2020).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Solar, G. E., Suer, O., Carpenter, T. O., Tan, C. D. & Li-Ng, M. Coronary heart failure in hypophosphatemic rickets: problems from high-dose phosphate remedy. Endocr. Pract. 19, e8–e11 (2013).

    PubMed 
    Article 

    Google Scholar
     

  • Currarino, G. Sagittal synostosis in X-linked hypophosphatemic rickets and associated illnesses. Pediatr. Radiol. 37, 805–812 (2007).

    PubMed 
    Article 

    Google Scholar
     

  • Glass, L. R., Dagi, T. F. & Dagi, L. R. Papilledema within the setting of x-linked hypophosphatemic rickets with craniosynostosis. Case Rep. Ophthalmol. 2, 376–381 (2011).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Rothenbuhler, A. et al. Excessive incidence of cranial synostosis and Chiari I malformation in youngsters with X-linked hypophosphatemic rickets (XLHR). J. Bone Min. Res. 34, 490–496 (2019).

    CAS 
    Article 

    Google Scholar
     

  • Christie, P. T., Harding, B., Nesbit, M. A., Whyte, M. P. & Thakker, R. V. X-linked hypophosphatemia attributable to pseudoexons of the PHEX gene. J. Clin. Endocrinol. Metab. 86, 3840–3844 (2001).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Harrell, R. M., Lyles, Ok. W., Harrelson, J. M., Friedman, N. E. & Drezner, M. Ok. Therapeutic of bone illness in X-linked hypophosphatemic rickets/osteomalacia. Induction and upkeep with phosphorus and calcitriol. J. Clin. Make investments. 75, 1858–1868 (1985).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Imel, E. A. et al. Burosumab versus standard remedy in youngsters with X-linked hypophosphataemia: a randomised, active-controlled, open-label, section 3 trial. Lancet 393, 2416–2427 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Kinoshita, Y. & Fukumoto, S. X-Linked Hypophosphatemia and FGF23-Associated hypophosphatemic illnesses: prospect for brand new therapy. Endocr. Rev. 39, 274–291 (2018).

    PubMed 
    Article 

    Google Scholar
     

  • Huiming, Y. & Chaomin, W. Recombinant progress hormone remedy for X-linked hypophosphatemia in youngsters. Cochrane Database Syst. Rev. https://doi.org/10.1002/14651858.CD004447.pub2 (2005).

    Article 
    PubMed 

    Google Scholar
     

  • Lecoq, A. L. et al. Hyperparathyroidism in Sufferers With X-Linked Hypophosphatemia. J. Bone Miner. Res. 35, 1263–1273 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Carpenter, T. O. The increasing household of hypophosphatemic syndromes. J. Bone Min. Metab. 30, 1–9 (2012).

    CAS 
    Article 

    Google Scholar
     

  • Econs, M. J. & McEnery, P. T. Autosomal dominant hypophosphatemic rickets/osteomalacia: medical characterization of a novel renal phosphate-wasting dysfunction. J. Clin. Endocrinol. Metab. 82, 674–681 (1997).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Imel, E. A., Biggin, A., Schindeler, A. & Munns, C. F. FGF23, hypophosphatemia, and rising remedies. JBMR Plus 3, e10190 (2019).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Imel, E. A. et al. Iron modifies plasma FGF23 in another way in autosomal dominant hypophosphatemic rickets and wholesome people. J. Clin. Endocrinol. Metab. 96, 3541–3549 (2011).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Rutsch, F. et al. Mutations in ENPP1 are related to ‘idiopathic’ childish arterial calcification. Nat. Genet. 34, 379–381 (2003).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Levy-Litan, V. et al. Autosomal-recessive hypophosphatemic rickets is related to an inactivation mutation within the ENPP1 gene. Am. J. Hum. Genet. 86, 273–278 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Alon, U. S. Medical follow. Fibroblast progress issue (FGF)23: a brand new hormone. Eur. J. Pediatr. 170, 545–554 (2011).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Liu, T. et al. DMP1 ablation within the rabbit ends in mineralization defects and abnormalities in Haversian canal/osteon microarchitecture. J. Bone Min. Res. 34, 1115–1128 (2019).

    CAS 
    Article 

    Google Scholar
     

  • Ferreira, C. R. et al. Potential phenotyping of long-term survivors of generalized arterial calcification of infancy (GACI). Genet. Med. 23, 396–407 (2021).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Jaureguiberry, G., Carpenter, T. O., Forman, S., Juppner, H. & Bergwitz, C. A novel missense mutation in SLC34A3 that causes hereditary hypophosphatemic rickets with hypercalciuria in people identifies threonine 137 as an vital determinant of sodium-phosphate cotransport in NaPi-IIc. Am. J. Physiol. Ren. Physiol. 295, F371–F379 (2008).

    CAS 
    Article 

    Google Scholar
     

  • Lorenz-Depiereux, B. et al. Hereditary hypophosphatemic rickets with hypercalciuria is attributable to mutations within the sodium-phosphate cotransporter gene SLC34A3. Am. J. Hum. Genet. 78, 193–201 (2006).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Bergwitz, C. & Miyamoto, Ok. I. Hereditary hypophosphatemic rickets with hypercalciuria: pathophysiology, medical presentation, analysis and remedy. Pflug. Arch. 471, 149–163 (2019).

    CAS 
    Article 

    Google Scholar
     

  • Haito-Sugino, S. et al. Processing and stability of sort IIc sodium-dependent phosphate cotransporter mutations in sufferers with hereditary hypophosphatemic rickets with hypercalciuria. Am. J. Physiol. Cell Physiol. 302, C1316–C1330 (2012).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Incorrect, O. M., Norden, A. G. & Feest, T. G. Dent’s illness; a familial proximal renal tubular syndrome with low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, metabolic bone illness, progressive renal failure and a marked male predominance. QJM 87, 473–493 (1994).

    CAS 
    PubMed 

    Google Scholar
     

  • Devuyst, O. & Thakker, R. V. Dent’s illness. Orphanet J. Uncommon Dis. 5, 28 (2010).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Hoopes, R. R. Jr. et al. Dent illness with mutations in OCRL1. Am. J. Hum. Genet. 76, 260–267 (2005).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Florenzano, P. et al. Tumor-induced osteomalacia. Calcif. Tissue Int. 108, 128–142 (2021).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Lee, J. C. et al. Characterization of FN1-FGFR1 and novel FN1-FGF1 fusion genes in a big sequence of phosphaturic mesenchymal tumors. Mod. Pathol. 29, 1335–1346 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Endo, I. et al. Nationwide survey of fibroblast progress issue 23 (FGF23)-related hypophosphatemic illnesses in Japan: prevalence, biochemical knowledge and therapy. Endocr. J. 62, 811–816 (2015).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Jiang, Y. et al. Tumor-induced osteomalacia: an vital explanation for adult-onset hypophosphatemic osteomalacia in China: Report of 39 circumstances and overview of the literature. J. Bone Min. Res. 27, 1967–1975 (2012).

    Article 

    Google Scholar
     

  • Minisola, S. et al. Tumour-induced osteomalacia. Nat. Rev. Dis. Prim. 3, 17044 (2017).

    PubMed 
    Article 

    Google Scholar
     

  • Wang, H. et al. Overexpression of fibroblast progress issue 23 suppresses osteoblast differentiation and matrix mineralization in vitro. J. Bone Min. Res. 23, 939–948 (2008).

    CAS 
    Article 

    Google Scholar
     

  • Brandi, M. L. et al. Challenges within the administration of tumor-induced osteomalacia (TIO). Bone 152, 116064 (2021).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Hartley, I. R. et al. Focused FGFR blockade for the therapy of tumor-induced osteomalacia. N. Engl. J. Med. 383, 1387–1389 (2020).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Ketteler, M., Gross, M. L. & Ritz, E. Calcification and cardiovascular issues in renal failure. Kidney Int. Suppl. https://doi.org/10.1111/j.1523-1755.2005.09428.x (2005).

    Article 
    PubMed 

    Google Scholar
     

  • Ramnitz, M. S., Gafni, R. I. & Collins, M. T. in GeneReviews Vol. NBK476672 (eds M. P. Adam et al.) (College of Washington, 2018).

  • Topaz, O. et al. Mutations in GALNT3, encoding a protein concerned in O-linked glycosylation, trigger familial tumoral calcinosis. Nat. Genet 36, 579–581 (2004).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Benet-Pages, A., Orlik, P., Strom, T. M. & Lorenz-Depiereux, B. An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia. Hum. Mol. Genet. 14, 385–390 (2005).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Ichikawa, S. et al. A homozygous missense mutation in human KLOTHO causes extreme tumoral calcinosis. J. Clin. Make investments. 117, 2684–2691 (2007).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Roberts, M. S. et al. Autoimmune hyperphosphatemic tumoral calcinosis in a affected person with FGF23 autoantibodies. J. Clin. Make investments. 128, 5368–5373 (2018).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Ramnitz, M. S., Gafni, R. I. & Collins, M. T. in GeneReviews Vol. NBK476672 (eds M. P. Adam et al.) (College of Washington, 2018).

  • Ramnitz, M. S. et al. Phenotypic and genotypic characterization and therapy of a cohort with familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome. J. Bone Min. Res. 31, 1845–1854 (2016).

    CAS 
    Article 

    Google Scholar
     

  • Clerin, V. et al. Selective pharmacological inhibition of the sodium-dependent phosphate cotransporter NPT2a promotes phosphate excretion. J. Clin. Make investments. 130, 6510–6522 (2020).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Mannstadt, M. et al. Hypoparathyroidism. Nat. Rev. Dis. Prim. 3, 17055 (2017).

    PubMed 
    Article 

    Google Scholar
     

  • Bilezikian, J. P. et al. Administration of hypoparathyroidism: current and future. J. Clin. Endocrinol. Metab. 101, 2313–2324 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Underbjerg, L., Sikjaer, T. & Rejnmark, L. Lengthy-term problems in sufferers with hypoparathyroidism evaluated by biochemical findings: a case-control examine. J. Bone Min. Res. 33, 822–831 (2018).

    CAS 
    Article 

    Google Scholar
     

  • Topaz, O. et al. A deleterious mutation in SAMD9 causes normophosphatemic familial tumoral calcinosis. Am. J. Hum. Genet. 79, 759–764 (2006).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Levine, M. A. Prognosis and administration of vitamin D dependent rickets. Entrance. Pediatr. 8, 315 (2020).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Gara, N. et al. Renal tubular dysfunction throughout long-term adefovir or tenofovir remedy in persistent hepatitis B. Aliment. Pharmacol. Ther. 35, 1317–1325 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Gray, A. et al. Low-dose fluoride in postmenopausal ladies: a randomized managed trial. J. Clin. Endocrinol. Metab. 98, 2301–2307 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Jha, S. Ok., Mishra, V. Ok., Sharma, D. Ok. & Damodaran, T. Fluoride within the surroundings and its metabolism in people. Rev. Env. Contam. Toxicol. 211, 121–142 (2011).

    CAS 

    Google Scholar
     

  • Chen, J. et al. Coal utilization in China: environmental impacts and human well being. Env. Geochem. Well being 36, 735–753 (2014).

    CAS 
    Article 

    Google Scholar
     

  • Majumdar, Ok. Ok. Well being influence of supplying protected ingesting water containing fluoride under permissible stage on flourosis sufferers in a fluoride-endemic rural space of West Bengal. Indian. J. Public Well being 55, 303–308 (2011).

    PubMed 
    Article 

    Google Scholar
     

  • Mousny, M. et al. Fluoride results on bone formation and mineralization are influenced by genetics. Bone 43, 1067–1074 (2008).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Pramanik, S. & Saha, D. The genetic affect in fluorosis. Env. Toxicol. Pharmacol. 56, 157–162 (2017).

    CAS 
    Article 

    Google Scholar
     

  • Tamer, M. N. et al. Osteosclerosis because of endemic fluorosis. Sci. Complete. Env. 373, 43–48 (2007).

    CAS 
    Article 

    Google Scholar
     

  • Pei, J. et al. Fluoride decreased osteoclastic bone resorption by means of the inhibition of NFATc1 gene expression. Env. Toxicol. 29, 588–595 (2014).

    CAS 
    Article 

    Google Scholar
     

  • Liu, Q. et al. Evaluation of the function of insulin signaling in bone turnover induced by fluoride. Biol. Hint Elem. Res. 171, 380–390 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Teotia, S. P. S., Teotia, M., Singh, Ok. P. & India. in 4th Worldwide Workshop on Fluorosis Prevention and Defluoridation of Water (ed. Dahi, E.) (The Worldwide Society for Fluoride Analysis, 2004).

  • Khairnar, M. R., Dodamani, A. S., Jadhav, H. C., Naik, R. G. & Deshmukh, M. A. Mitigation of fluorosis — a overview. J. Clin. Diagn. Res. 9, ZE05–ZE09 (2015).

    PubMed 
    PubMed Central 

    Google Scholar
     

  • Mulay, S. R. & Anders, H. J. Crystallopathies. N. Engl. J. Med. 374, 2465–2476 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Munoz, L. E. et al. Neutrophil extracellular traps provoke gallstone formation. Immunity 51, 443–450.e444 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Chiti, F. & Dobson, C. M. Protein misfolding, amyloid formation, and human illness: a abstract of progress during the last decade. Annu. Rev. Biochem. 86, 27–68 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mulay, S. R., Steiger, S., Shi, C. & Anders, H. J. A information to crystal-related and nano- or microparticle-related tissue responses. FEBS J. 287, 818–832 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Kzhyshkowska, J. et al. Macrophage responses to implants: prospects for personalised drugs. J. Leukoc. Biol. 98, 953–962 (2015).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Sheikh, Z., Brooks, P. J., Barzilay, O., Fantastic, N. & Glogauer, M. Macrophages, overseas physique large cells and their response to implantable biomaterials. Supplies 8, 5671–5701 (2015).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Wang, F., Gomez-Sintes, R. & Boya, P. Lysosomal membrane permeabilization and cell dying. Site visitors 19, 918–931 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Franklin, B. S., Mangan, M. S. & Latz, E. Crystal formation in irritation. Annu. Rev. Immunol. 34, 173–202 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Martinon, F., Petrilli, V., Mayor, A., Tardivel, A. & Tschopp, J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 440, 237–241 (2006).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mulay, S. R. et al. Mitochondria permeability transition versus necroptosis in oxalate-induced AKI. J. Am. Soc. Nephrol. 30, 1857–1869 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Schauer, C. et al. Aggregated neutrophil extracellular traps restrict irritation by degrading cytokines and chemokines. Nat. Med. 20, 511–517 (2014).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Desai, J. et al. Particles of various dimensions and shapes induce neutrophil necroptosis adopted by the discharge of neutrophil extracellular trap-like chromatin. Sci. Rep. 7, 15003 (2017).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Desai, J. et al. PMA and crystal-induced neutrophil extracellular lure formation includes RIPK1-RIPK3-MLKL signaling. Eur. J. Immunol. 46, 223–229 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shi, C. et al. Crystal clots as therapeutic goal in ldl cholesterol crystal embolism. Circ. Res. 126, e37–e52 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mulay, S. R. & Anders, H. J. Crystal nephropathies: mechanisms of crystal-induced kidney damage. Nat. Rev. Nephrol. 13, 226–240 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Worcester, E. M. & Coe, F. L. Medical follow. Calcium kidney stones. N. Engl. J. Med. 363, 954–963 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Mulay, S. R. & Anders, H. J. Crystallopathies. N. Engl. J. Med. 375, e29 (2016).

    PubMed 
    Article 

    Google Scholar
     

  • Mahajan, A. et al. Frontline science: aggregated neutrophil extracellular traps forestall irritation on the neutrophil-rich ocular floor. J. Leukoc. Biol. 105, 1087–1098 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Asselman, M., Verhulst, A., De Broe, M. E. & Verkoelen, C. F. Calcium oxalate crystal adherence to hyaluronan-, osteopontin-, and CD44-expressing injured/regenerating tubular epithelial cells in rat kidneys. J. Am. Soc. Nephrol 14, 3155–3166 (2003).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mulay, S. R. et al. Hyperoxaluria requires TNF receptors to provoke crystal adhesion and kidney stone illness. J. Am. Soc. Nephrol. 28, 761–768 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Cochat, P. & Rumsby, G. Major hyperoxaluria. N. Engl. J. Med. 369, 649–658 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Kletzmayr, A. et al. Inhibitors of calcium oxalate crystallization for the therapy of oxalate nephropathies. Adv. Sci. 7, 1903337 (2020).

    CAS 
    Article 

    Google Scholar
     

  • Marschner, J. A. et al. The lengthy pentraxin PTX3 is an endogenous inhibitor of hyperoxaluria-related nephrocalcinosis and persistent kidney illness. Entrance. Immunol. 9, 2173 (2018).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Steiger, S. et al. Anti-transforming progress issue beta IgG elicits a twin impact on calcium oxalate crystallization and progressive nephrocalcinosis-related persistent kidney illness. Entrance. Immunol. 9, 619 (2018).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Duewell, P. et al. NLRP3 inflammasomes are required for atherogenesis and activated by ldl cholesterol crystals. Nature 464, 1357–1361 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Mulay, S. R., Evan, A. & Anders, H. J. Molecular mechanisms of crystal-related kidney irritation and damage. Implications for ldl cholesterol embolism, crystalline nephropathies and kidney stone illness. Nephrol. Dialysis Transpl. 29, 507–514 (2014).

    CAS 
    Article 

    Google Scholar
     

  • Lautenschlager, S. O. S. et al. Plasma proteins and platelets modulate neutrophil clearance of malaria-related hemozoin crystals. Cells https://doi.org/10.3390/cells9010093 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kumar, R., Tebben, P. J. & Thompson, J. R. Vitamin D and the kidney. Arch. Biochem. Biophys. 523, 77–86 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Tebben, P. J., Singh, R. J. & Kumar, R. Vitamin D-mediated hypercalcemia: mechanisms, analysis, and therapy. Endocr. Rev. 37, 521–547 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Zand, L. & Kumar, R. Using vitamin d metabolites and analogues within the therapy of persistent kidney illness. Endocrinol. Metab. Clin. North. Am. 46, 983–1007 (2017).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Silver, J. & Levi, R. Regulation of PTH synthesis and secretion related to the administration of secondary hyperparathyroidism in persistent kidney illness. Kidney Int. Suppl. 95, S8–S12 (2005).

    CAS 
    Article 

    Google Scholar
     

  • Silver, J. & Levi, R. Mobile and molecular mechanisms of secondary hyperparathyroidism. Clin. Nephrol. 63, 119–126 (2005).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Lieske, J. C. et al. Renal stone epidemiology in Rochester, Minnesota: an replace. Kidney Int. 69, 760–764 (2006).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Curhan, G. C. Epidemiology of stone illness. Urol. Clin. North. Am. 34, 287–293 (2007).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Curhan, G. C., Rimm, E. B., Willett, W. C. & Stampfer, M. J. Regional variation in nephrolithiasis incidence and prevalence amongst United States males. J. Urol. 151, 838–841 (1994).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Park, S. & Pearle, M. S. Pathophysiology and administration of calcium stones. Urol. Clin. North. Am. 34, 323–334 (2007).

    PubMed 
    Article 

    Google Scholar
     

  • Broadus, A. E. et al. A consideration of the hormonal foundation and phosphate leak speculation of absorptive hypercalciuria. J. Clin. Endocrinol. Metab. 58, 161–169 (1984).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Cupisti, A. et al. Serum calcitriol and dietary protein consumption in idiopathic calcium stone sufferers. Int. J. Clin. Lab. Res. 29, 85–88 (1999).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Frick, Ok. Ok. et al. 1,25(OH)(2)D(3)-enhanced hypercalciuria in genetic hypercalciuric stone-forming rats fed a low-calcium weight-reduction plan. Am. J. Physiol. Ren. Physiol. 305, F1132–F1138 (2013).

    CAS 
    Article 

    Google Scholar
     

  • Giannini, S. et al. Doable hyperlink between vitamin D and hyperoxaluria in sufferers with renal stone illness. Clin. Sci. 84, 51–54 (1993).

    CAS 
    Article 

    Google Scholar
     

  • Ketha, H. et al. Altered calcium and vitamin D homeostasis in first-time calcium kidney stone-formers. PLoS One 10, e0137350 (2015).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Lieske, J. C. et al. Stone composition as a perform of age and intercourse. Clin. J. Am. Soc. Nephrol. 9, 2141–2146 (2014).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Singh, P. et al. Stone composition amongst first-time symptomatic kidney stone formers locally. Mayo Clin. Proc. 90, 1356–1365 (2015).

    PubMed 
    Article 

    Google Scholar
     

  • Evan, A., Lingeman, J., Coe, F. L. & Worcester, E. Randall’s plaque: pathogenesis and function in calcium oxalate nephrolithiasis. Kidney Int. 69, 1313–1318 (2006).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Evan, A. P. et al. Randall’s plaque of sufferers with nephrolithiasis begins in basement membranes of skinny loops of Henle. J. Clin. Make investments. 111, 607–616 (2003).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Krambeck, A. E. et al. Present computed tomography strategies can detect duct of Bellini plugging however not Randall’s plaques. Urology 82, 301–306 (2013).

    PubMed 
    Article 

    Google Scholar
     

  • Linnes, M. P. et al. Phenotypic characterization of kidney stone formers by endoscopic and histological quantification of intrarenal calcification. Kidney Int. 84, 818–825 (2013).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Matlaga, B. R., Coe, F. L., Evan, A. P. & Lingeman, J. E. The function of Randall’s plaques within the pathogenesis of calcium stones. J. Urol. 177, 31–38 (2007).

    PubMed 
    Article 

    Google Scholar
     

  • Lieske, J. C., Turner, S. T., Edeh, S. N., Smith, J. A. & Kardia, S. L. Heritability of urinary traits that contribute to nephrolithiasis. Clin. J. Am. Soc. Nephrol. 9, 943–950 (2014).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Lieske, J. C. et al. Heritability of dietary traits that contribute to nephrolithiasis in a cohort of grownup sibships. J. Nephrol. 29, 45–51 (2016).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Lieske, J. C. & Wang, X. Heritable traits that contribute to nephrolithiasis. Urolithiasis 47, 5–10 (2019).

    PubMed 
    Article 

    Google Scholar
     

  • Arcidiacono, T. et al. Idiopathic calcium nephrolithiasis: a overview of pathogenic mechanisms within the mild of genetic research. Am. J. Nephrol. 40, 499–506 (2014).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Gudbjartsson, D. F. et al. Affiliation of variants at UMOD with persistent kidney illness and kidney stones-role of age and comorbid illnesses. PLoS Genet. 6, e1001039 (2010).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Howles, S. A. et al. Genetic variants of calcium and vitamin D metabolism in kidney stone illness. Nat. Commun. 10, 5175 (2019).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Okada, A. et al. Genome-wide evaluation of genes associated to kidney stone formation and elimination within the calcium oxalate nephrolithiasis mannequin mouse: detection of stone-preventive elements and involvement of macrophage exercise. J. Bone Min. Res. 24, 908–924 (2009).

    CAS 
    Article 

    Google Scholar
     

  • Palsson, R., Indridason, O. S., Edvardsson, V. O. & Oddsson, A. Genetics of frequent advanced kidney stone illness: insights from genome-wide affiliation research. Urolithiasis 47, 11–21 (2019).

    PubMed 
    Article 

    Google Scholar
     

  • Rungroj, N. et al. An entire genome SNP genotyping by DNA microarray and candidate gene affiliation examine for kidney stone illness. BMC Med. Genet. 15, 50 (2014).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Taguchi, Ok. et al. Genome-wide gene expression profiling of Randall’s plaques in calcium oxalate stone formers. J. Am. Soc. Nephrol. 28, 333–347 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Taguchi, Ok., Yasui, T., Milliner, D. S., Hoppe, B. & Chi, T. Genetic danger elements for idiopathic urolithiasis: a scientific overview of the literature and causal community evaluation. Eur. Urol. Focus 3, 72–81 (2017).

    PubMed 
    Article 

    Google Scholar
     

  • Thorleifsson, G. et al. Sequence variants within the CLDN14 gene affiliate with kidney stones and bone mineral density. Nat. Genet. 41, 926–930 (2009).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Urabe, Y. et al. A genome-wide affiliation examine of nephrolithiasis within the Japanese inhabitants identifies novel inclined Loci at 5q35.3, 7p14.3, and 13q14.1. PLoS Genet. 8, e1002541 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Vezzoli, G., Terranegra, A., Arcidiacono, T. & Soldati, L. Genetics and calcium nephrolithiasis. Kidney Int. 80, 587–593 (2011).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • O’Keeffe, D. T. et al. Medical and biochemical phenotypes of adults with monoallelic and biallelic CYP24A1 mutations: proof of gene dose impact. Osteoporos. Int. 27, 3121–3125 (2016).

    PubMed 
    Article 
    CAS 

    Google Scholar
     

  • Tebben, P. J. et al. Hypercalcemia, hypercalciuria, and elevated calcitriol concentrations with autosomal dominant transmission because of CYP24A1 mutations: results of ketoconazole remedy. J. Clin. Endocrinol. Metab. 97, E423–E427 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Thompson, B. & Towler, D. A. Arterial calcification and bone physiology: function of the bone-vascular axis. Nat. Rev. Endocrinol. 8, 529–543 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Leibowitz, J. O. The Historical past of Coronary Coronary heart Illness (Wellcome Institute of the Historical past of Medication, 1970).

  • Towler, D. A. Commonalities between vasculature and bone: an osseocentric view of arteriosclerosis. Circulation 135, 320–322 (2017).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Stabley, J. N. & Towler, D. A. Arterial calcification in diabetes mellitus: preclinical fashions and translational implications. Arterioscler. Thromb. Vasc. Biol. 37, 205–217 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Speer, M. Y. et al. Clean muscle cells give rise to osteochondrogenic precursors and chondrocytes in calcifying arteries. Circ. Res. 104, 733–741 (2009).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Bennett, M. R., Sinha, S. & Owens, G. Ok. Vascular clean muscle cells in aherosclerosis. Circ. Res. 118, 692–702 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Pederson, L., Ruan, M., Westendorf, J. J., Khosla, S. & Oursler, M. J. Regulation of bone formation by osteoclasts includes Wnt/BMP signaling and the chemokine sphingosine-1-phosphate. Proc. Natl Acad. Sci. USA 105, 20764–20769 (2008).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Stefater, J. A. third et al. Macrophage Wnt-Calcineurin-Flt1 signaling regulates mouse wound angiogenesis and restore. Blood 121, 2574–2578 (2013).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Demer, L. L. & Tintut, Y. Inflammatory, metabolic, and genetic mechanisms of vascular calcification. Arterioscler. Thromb. Vasc. Biol. 34, 715–723 (2014).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Cheng, S. L. et al. Focused discount of vascular Msx1 and Msx2 mitigates arteriosclerotic calcification and aortic stiffness in LDLR-deficient mice fed diabetogenic diets. Diabetes 63, 4326–4337 (2014).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Solar, Y. et al. Clean muscle cell-specific runx2 deficiency inhibits vascular calcification. Circ. Res. 111, 543–552 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Dillon, S., Staines, Ok. A., Millan, J. L. & Farquharson, C. The best way to construct a bone: PHOSPHO1, biomineralization, and past. JBMR 3, e10202 (2019).


    Google Scholar
     

  • Duer, M., Cobb, A. M. & Shanahan, C. M. DNA harm response: a molecular lynchpin within the pathobiology of arteriosclerotic calcification. Arterioscler. Thromb. Vasc. Biol. 40, e193–e202 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Croft, M. & Siegel, R. M. Past TNF: TNF superfamily cytokines as targets for the therapy of rheumatic illnesses. Nat. Rev. Rheumatol. 13, 217–233 (2017).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Cheng, S. L. et al. Activation of vascular clean muscle parathyroid hormone receptor inhibits Wnt/beta-catenin signaling and aortic fibrosis in diabetic arteriosclerosis. Circ. Res. 107, 271–282 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Jilka, R. L. et al. Decreased oxidative stress and larger bone anabolism within the aged, when in comparison with the younger, murine skeleton with parathyroid hormone administration. Ageing Cell 9, 851–867 (2010).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Behrmann, A. et al. PTH/PTHrP receptor signaling restricts arterial fibrosis in diabetic LDLR(-/-) mice by inhibiting myocardin-related transcription issue relays. Circ. Res. 126, 1363–1378 (2020).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Raison, D. et al. Knockdown of parathyroid hormone associated protein in clean muscle cells alters renal hemodynamics however not blood strain. Am. J. Physiol. Ren. Physiol. 305, F333–F342 (2013).

    CAS 
    Article 

    Google Scholar
     

  • Yu, N. et al. Elevated mortality and morbidity in gentle main hyperparathyroid sufferers. The Parathyroid Epidemiology and Audit Analysis Examine (PEARS). Clin. Endocrinol. 73, 30–34 (2010).


    Google Scholar
     

  • Nyby, M. D. et al. Desensitization of vascular tissue to parathyroid hormone and parathyroid hormone-related protein. Endocrinology 136, 2497–2504 (1995).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shao, J. S., Cheng, S. L., Sadhu, J. & Towler, D. A. Irritation and the osteogenic regulation of vascular calcification: a overview and perspective. Hypertension 55, 579–592 (2010).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Zheng, Ok. H. et al. Lipoprotein(a) and oxidized phospholipids promote valve calcification in sufferers with aortic stenosis. J. Am. Coll. Cardiol. 73, 2150–2162 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Elmariah, S. et al. Bisphosphonate use and prevalence of valvular and vascular calcification in ladies MESA (The Multi-Ethnic Examine of Atherosclerosis). J. Am. Coll. Cardiol. 56, 1752–1759 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Xiang, Z. et al. Focused activation of human Vgamma9Vdelta2-T cells controls Epstein-Barr virus-induced B cell lymphoproliferative illness. Most cancers Cell 26, 565–576 (2014).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Sing, C. W. et al. Affiliation of alendronate and danger of cardiovascular occasions in sufferers with hip fracture. J. Bone Min. Res. 33, 1422–1434 (2018).

    CAS 
    Article 

    Google Scholar
     

  • Saag, Ok. G. et al. Romosozumab or alendronate for fracture prevention in ladies with osteoporosis. N. Engl. J. Med. 377, 1417–1427 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shao, J. S. et al. Msx2 promotes cardiovascular calcification by activating paracrine Wnt indicators. J. Clin. Make investments. 115, 1210–1220 (2005).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Krishna, S. M. et al. Wnt signaling pathway inhibitor sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 37, 553–566 (2017).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Shoback, D. et al. Pharmacological administration of osteoporosis in postmenopausal ladies: an endocrine society guideline replace. J. Clin. Endocrinol. Metab. 105, dgaa048 (2020).

    PubMed 
    Article 

    Google Scholar
     

  • Lanske, B. et al. Ablation of the PTHrP gene or the PTH/PTHrP receptor gene results in distinct abnormalities in bone improvement. J. Clin. Make investments. 104, 399–407 (1999).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Gardinier, J. D., Daly-Seiler, C., Rostami, N., Kundal, S. & Zhang, C. Lack of the PTH/PTHrP receptor alongside the osteoblast lineage limits the anabolic response to train. PLoS One 14, e0211076 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Whyte, M. P. et al. New clarification for autosomal dominant excessive bone mass: mutation of low-density lipoprotein receptor-related protein 6. Bone 127, 228–243 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Li, C. et al. Disruption of LRP6 in osteoblasts blunts the bone anabolic exercise of PTH. J. Bone Min. Res. 28, 2094–2108 (2013).

    CAS 
    Article 

    Google Scholar
     

  • Cheng, S. L. et al. Vascular clean muscle LRP6 limits arteriosclerotic calcification in diabetic LDLR-/- mice by restraining noncanonical Wnt indicators. Circ. Res. 117, 142–156 (2015).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Cauley, J. A. Public well being influence of osteoporosis. J. Gerontol. A Biol. Sci. Med. Sci. 68, 1243–1251 (2013).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • American Coronary heart Affiliation. Coronary heart and Stroke Statistics. www.coronary heart.org. https://www.coronary heart.org/en/about-us/heart-and-stroke-association-statistics (2020).

  • Veronese, N. et al. Relationship between low bone mineral density and fractures with incident heart problems: a scientific overview and meta-analysis. J. Bone Min. Res. 32, 1126–1135 (2017).

    Article 

    Google Scholar
     

  • Chiang, C. H. et al. Hip fracture and danger of acute myocardial infarction: a nationwide examine. J. Bone Min. Res. 28, 404–411 (2013).

    Article 

    Google Scholar
     

  • Zhou, R., Zhou, H., Cui, M., Chen, L. & Xu, J. The affiliation between aortic calcification and fracture danger in postmenopausal ladies in China: the potential Chongqing osteoporosis examine. PLoS One 9, e93882 (2014).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Szulc, P. et al. Belly aortic calcification and danger of fracture amongst older ladies — the SOF examine. Bone 81, 16–23 (2015).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Chan, J. J. et al. QCT volumetric bone mineral density and vascular and valvular calcification: the Framingham examine. J. Bone Min. Res. 30, 1767–1774 (2015).

    Article 

    Google Scholar
     

  • Wei, D., Zheng, G., Gao, Y., Guo, J. & Zhang, T. Belly aortic calcification and the chance of bone fractures: a meta-analysis of potential cohort research. J. Bone Min. Metab. 36, 439–446 (2018).

    CAS 
    Article 

    Google Scholar
     

  • Caffarelli, C., Montagnani, A., Nuti, R. & Gonnelli, S. Bisphosphonates, atherosclerosis and vascular calcification: replace and systematic overview of medical research. Clin. Interv. Ageing 12, 1819–1828 (2017).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Szulc, P., Samelson, E. J., Kiel, D. P. & Delmas, P. D. Elevated bone resorption is related to elevated danger of cardiovascular occasions in males: the MINOS examine. J. Bone Min. Res. 24, 2023–2031 (2009).

    CAS 
    Article 

    Google Scholar
     

  • Cauley, J. A. et al. Inflammatory markers and the chance of hip and vertebral fractures in males: the osteoporotic fractures in males (MrOS). J. Bone Min. Res. 31, 2129–2138 (2016).

    CAS 
    Article 

    Google Scholar
     

  • Barbour, Ok. E. et al. Inflammatory markers and danger of hip fracture in older white ladies: the examine of osteoporotic fractures. J. Bone Min. Res. 29, 2057–2064 (2014).

    CAS 
    Article 

    Google Scholar
     

  • Choi, H. J. et al. Danger of fractures in topics with antihypertensive medicines: a nationwide declare examine. Int. J. Cardiol. 184, 62–67 (2015).

    PubMed 
    Article 

    Google Scholar
     

  • Swanson, C. M. et al. Obstructive sleep apnea and metabolic bone illness: insights into the connection between bone and sleep. J. Bone Min. Res. 30, 199–211 (2015).

    Article 

    Google Scholar
     

  • Cauley, J. A. et al. Traits of self-reported sleep and the chance of falls and fractures: the Ladies’s Well being Initiative (WHI). J. Bone Min. Res. 34, 464–474 (2019).

    CAS 
    Article 

    Google Scholar
     

  • Cauley, J. A. et al. Hypoxia throughout sleep and the chance of falls and fractures in older males: the Osteoporotic Fractures in Males Sleep Examine. J. Am. Geriatr. Soc. 62, 1853–1859 (2014).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Sullivan, S. D. et al. Results of self-reported age at nonsurgical menopause on time to first fracture and bone mineral density within the Ladies’s Well being Initiative Observational Examine. Menopause 22, 1035–1044 (2015).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Muka, T. et al. Affiliation of age at onset of menopause and time since onset of menopause with cardiovascular outcomes, intermediate vascular traits, and all-cause mortality: a scientific overview and meta-analysis. JAMA Cardiol. 1, 767–776 (2016).

    PubMed 
    Article 

    Google Scholar
     

  • D’Amelio, P. et al. Function of iron metabolism and oxidative harm in postmenopausal bone loss. Bone 43, 1010–1015 (2008).

    PubMed 
    Article 
    CAS 

    Google Scholar
     

  • McLean, R. R. et al. Homocysteine as a predictive issue for hip fracture in older individuals. N. Engl. J. Med. 350, 2042–2049 (2004).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Pusceddu, I. et al. Subclinical irritation, telomere shortening, homocysteine, vitamin B6, and mortality: the Ludwigshafen Danger and Cardiovascular Well being Examine. Eur. J. Nutr. 59, 1399–1411 (2019).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar
     

  • Wang, S. et al. Prevalence and extent of calcification over aorta, coronary and carotid arteries in sufferers with rheumatoid arthritis. J. Intern. Med. 266, 445–452 (2009).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • Mackey, R. H. et al. Rheumatoid arthritis, anti-cyclic citrullinated peptide positivity, and heart problems danger within the ladies’s well being initiative. Arthritis Rheumatol. 67, 2311–2322 (2015).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar
     

  • Singh, P., Harris, P. C., Sas, D. J. & Lieske, J. C. The genetics of kidney stone illness and nephrocalcinosis. Nat. Rev. Nephrol. 18, 224–240 (2022).

    PubMed 
    Article 

    Google Scholar
     

  • Mizobuchi, M., Towler, D. & Slatopolsky, E. Vascular calcification: the killer of sufferers with persistent kidney illness. J. Am. Soc. Nephrol. 20, 1453–1464 (2009).

    CAS 
    PubMed 
    Article 

    Google Scholar
     

  • RELATED ARTICLES

    Most Popular

    Recent Comments