The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Regulation and Function of the FGF23/Klotho Endocrine Pathways
Open accessAbstract
Calcium (Ca 2+) and phosphate (PO 43−) homeostasis are coordinated by systemic and local factors that regulate intestinal absorption, influx and efflux from bone, and kidney excretion and reabsorption of these ions through a complex hormonal network. Traditionally, the parathyroid hormone (PTH)/vitamin D axis provided the conceptual framework to understand mineral metabolism. PTH secreted by the parathyroid gland in response to hypocalcemia functions to maintain serum Ca 2+levels by increasing Ca 2+reabsorption and 1,25-dihydroxyvitamin D [1,25(OH)2 D] production by the kidney, enhancing Ca 2+and PO 43−intestinal absorption and increasing Ca 2+and PO 43−efflux from bone, while maintaining neutral phosphate balance through phosphaturic effects. FGF23 is a recently discovered hormone, predominately produced by osteoblasts/osteocytes, whose major functions are to inhibit renal tubular phosphate reabsorption and suppress circulating 1,25(OH)2 D levels by decreasing Cyp27b1-mediated formation and stimulating Cyp24-mediated catabolism of 1,25(OH)2 D. FGF23 participates in a new bone/kidney axis that protects the organism from excess vitamin D and coordinates renal PO 43−handling with bone mineralization/turnover. Abnormalities of FGF23 production underlie many inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts.
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Cites
Mutation of the mouse klotho gene leads to a syndrome resembling ageing
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Suppression of Aging in Mice by the Hormone Klotho
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“Estrogen deficiency is a major cause of osteoporosis as estrogens play a key role in balancing bone remodeling directly (127, 163) and indirectly through modulation of PTH, calcium, and vitamin D signaling (110, 151, 198).”
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“Inactivation of DMP1 also leads to increased Fgf23 expression in bone (40, 121, 122).”
Self-citationReceptor Specificity of the Fibroblast Growth Factor Family
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Endocrine functions of bone in mineral metabolism regulation
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The physiology of endocrine systems with ageing
van den Beld, A. W., Kaufman, J.-M., Zillikens, M. C., Lamberts, S. W. J., Egan, J. M., & van der Lely, A. J. (2018) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(18)30026-3 · Cited by 349
Therapeutic management of hypophosphatemic rickets from infancy to adulthood
Linglart, A., Biosse-Duplan, M., Briot, K., Chaussain, C., Esterle, L., Guillaume-Czitrom, S., Kamenicky, P., Nevoux, J., Prié, D., Rothenbuhler, A., et al. (2014) · Endocrine Connections · doi:10.1530/ec-13-0103 · Cited by 331
Protein nutrition and malnutrition in CKD and ESRD
Zha, Y., & Qian, Q. (2017) · Nutrients · doi:10.3390/nu9030208 · Cited by 292
Jin, L., Yang, R., Geng, L., & Xu, A. (2023) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-032322-093904 · Cited by 71
Metadata
- Authors
- Martin, A., David, V., & Quarles, L. D.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2012-01
- Volume
- 92
- Issue
- 1
- Pages
- 131-155
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2129321769
- Cited by
- 594
- References
- 14
- FWCI
- 5.76
- Type
- journal article
- Language
- en
- Open access
- green
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