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- W88081567 abstract "The fibroblast growth factor (FGF) family comprises a number of polypeptides which share a common homology core region. FGF-23, produced by osteoblasts and osteocytes, belongs to the FGF-19 subfamily and serves as the main phosphatonine. Two forms of circulating FGF-23 are detectable in serum: full-length FGF-23--intact FGF-23 (iFGF-23), which is biologically active, and the inactive C-terminal FGF-23 (cFGF-23). FGF-23 with a coreceptor (Klotho protein) inhibits renal phosphate reabsorption and synthesis of calcitriol by reducing 1alpha-hydroxylase (CYP27B1) activity, reducing vitamin D-dependent phosphate intestinal absorption. High phosphorus intake, 1,25-dihydroxyvitamin D3 and PTH are the main stimuli for FGF-23 secretion. Impaired FGF-23 metabolism is involved in phosphate disturbances manifesting as rickets or osteomalacia or increased tissue calcinosis. FGF-23 may be also produced by some tumors leading to hypophosphatemia. Both cFGF-23 and iFGF-23 concentrations start to increase with mild impairment of the glomerular filtration rate in stage 2 or 3 of chronic kidney disease (CKD) as a consequence of the increased FGF-23 production. It seems that enhanced FGF-23 secretion may constitute a protective mechanism against enhanced phosphate accumulation in the early stages of CKD. However, it may lead to calcitriol deficiency and escalation of secondary hyperparathyroidism. Increased FGF-23 level is supposed to be an independent factor increasing mortality of CKD patients. There is ambiguous data if FGF-23 only reflects disturbances in calcium-phosphate metabolism or if it exerts a detrimental effect itself by diminishing calcitriol synthesis, inducing cell proliferation or acting through low-affinity, Klotho-independent receptors in the heart and endothelium. So far, little evidence supports direct FGF-23 toxicity." @default.
- W88081567 created "2016-06-24" @default.
- W88081567 creator A5043245600 @default.
- W88081567 creator A5045517198 @default.
- W88081567 creator A5058104418 @default.
- W88081567 date "2012-12-12" @default.
- W88081567 modified "2023-09-29" @default.
- W88081567 title "Fibroblast growth factor 23--structure, function and role in kidney diseases." @default.
- W88081567 cites W1944551911 @default.
- W88081567 cites W1965113966 @default.
- W88081567 cites W1967918805 @default.
- W88081567 cites W1968779137 @default.
- W88081567 cites W1977645780 @default.
- W88081567 cites W1980355813 @default.
- W88081567 cites W1987998131 @default.
- W88081567 cites W1988032328 @default.
- W88081567 cites W1992157366 @default.
- W88081567 cites W2000665430 @default.
- W88081567 cites W2003490678 @default.
- W88081567 cites W2003632139 @default.
- W88081567 cites W2003963660 @default.
- W88081567 cites W2007546762 @default.
- W88081567 cites W2012675371 @default.
- W88081567 cites W2015668150 @default.
- W88081567 cites W2021852822 @default.
- W88081567 cites W2027418334 @default.
- W88081567 cites W2028415754 @default.
- W88081567 cites W2028480953 @default.
- W88081567 cites W2031941775 @default.
- W88081567 cites W2037498463 @default.
- W88081567 cites W2042639382 @default.
- W88081567 cites W2049229440 @default.
- W88081567 cites W2051731547 @default.
- W88081567 cites W2053425137 @default.
- W88081567 cites W2054151200 @default.
- W88081567 cites W2059022155 @default.
- W88081567 cites W2059115865 @default.
- W88081567 cites W2060108666 @default.
- W88081567 cites W2063765502 @default.
- W88081567 cites W2066517300 @default.
- W88081567 cites W2068249054 @default.
- W88081567 cites W2077703010 @default.
- W88081567 cites W2078522380 @default.
- W88081567 cites W2080387599 @default.
- W88081567 cites W2081257855 @default.
- W88081567 cites W2083288593 @default.
- W88081567 cites W2089724134 @default.
- W88081567 cites W2091948921 @default.
- W88081567 cites W2095948376 @default.
- W88081567 cites W2106711282 @default.
- W88081567 cites W2107207648 @default.
- W88081567 cites W2109177164 @default.
- W88081567 cites W2114360920 @default.
- W88081567 cites W2114372930 @default.
- W88081567 cites W2115776336 @default.
- W88081567 cites W2117624714 @default.
- W88081567 cites W2120129493 @default.
- W88081567 cites W2122584551 @default.
- W88081567 cites W2124070987 @default.
- W88081567 cites W2127999488 @default.
- W88081567 cites W2129739601 @default.
- W88081567 cites W2130362586 @default.
- W88081567 cites W2137259612 @default.
- W88081567 cites W2138178479 @default.
- W88081567 cites W2139356410 @default.
- W88081567 cites W2139989191 @default.
- W88081567 cites W2140430174 @default.
- W88081567 cites W2140575711 @default.
- W88081567 cites W2146666133 @default.
- W88081567 cites W2147380695 @default.
- W88081567 cites W2147734839 @default.
- W88081567 cites W2153237907 @default.
- W88081567 cites W2154287224 @default.
- W88081567 cites W2154614385 @default.
- W88081567 cites W2154900396 @default.
- W88081567 cites W2155014825 @default.
- W88081567 cites W2157448600 @default.
- W88081567 cites W2163648134 @default.
- W88081567 cites W2164533721 @default.
- W88081567 cites W2164952534 @default.
- W88081567 cites W2165433745 @default.
- W88081567 cites W2165894407 @default.
- W88081567 cites W2166915967 @default.
- W88081567 cites W2170092490 @default.
- W88081567 cites W2171055549 @default.
- W88081567 cites W2172122530 @default.
- W88081567 cites W2172200321 @default.
- W88081567 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23214203" @default.
- W88081567 hasPublicationYear "2012" @default.
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