作者
Christian Faul, Ansel P Amaral, Behzad Oskouei, Ming-Chang Hu, Alexis Sloan, Tamara Isakova, Orlando M Gutiérrez, Robier Aguillon-Prada, Joy Lincoln, Joshua M Hare, Peter Mundel, Azorides Morales, Julia Scialla, Michael Fischer, Elsayed Z Soliman, Jing Chen, Alan S Go, Sylvia E Rosas, Lisa Nessel, Raymond R Townsend, Harold I Feldman, Martin St John Sutton, Akinlolu Ojo, Crystal Gadegbeku, Giovana Seno Di Marco, Stefan Reuter, Dominik Kentrup, Klaus Tiemann, Marcus Brand, Joseph A Hill, Orson W Moe, Makoto Kuro-o, John W Kusek, Martin G Keane, Myles Wolf
发表日期
2011/10/10
期刊
The Journal of clinical investigation
卷号
121
期号
11
出版商
American Society for Clinical Investigation
简介
Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor–dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated …
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C Faul, AP Amaral, B Oskouei, MC Hu, A Sloan… - The Journal of clinical investigation, 2011