Is Circulating Fibroblast Growth Factor 23 a Surrogate Marker or Active Mediator for the Construction of Atrial Fibrillation Substrate?
Author:
Affiliation:
1. Department of Cardiovascular Medicine, Kitasato University School of Medicine
Publisher
Japanese Circulation Society
Subject
Cardiology and Cardiovascular Medicine,General Medicine
Link
https://www.jstage.jst.go.jp/article/circj/advpub/0/advpub_CJ-15-0506/_pdf
Reference17 articles.
1. 1. Gutierrez OM. Fibroblast growth factor 23, Klotho and disordered mineral metabolism in chronic kidney disease: Unraveling the intricate tapestry of events and implications for therapy. J Ren Nutr 2013; 23: 250–254.
2. 2. Quarles LD. Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism. Nat Rev Endocrinol 2012; 8: 276–286.
3. 3. Bowe AE, Finnegan R, Jan de Neur SM, Cho J, Levine MA, Kumar R, et al. FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate. Biochem Biophys Res Commun 2001; 284: 977–981.
4. 4. Ben-Dov IZ, Galitzer H, Lavi-Moshayoff V, Goetz R, Kuro-o M, Mohammadi M, et al. The parathyroid is a target organ for FGF23 in rats. J Clin Invest 2007; 117: 4003–4008.
5. 5. Shalhoub V, Shatzen EM, Ward SC, Davis J, Stevens J, Bi V, et al. FGF23 neutralization improves chronic kidney disease associated hyperparathyroidism yet increases mortality. J Clin Invest 2012; 122: 2543–2553.
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1. Predictive value of circulating fibroblast growth factor-23 on atrial fibrillation: A meta-analysis;International Journal of Cardiology;2016-05
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