Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/138502
Title: FGF21 and cardiac Physiopathology
Author: Planavila Porta, Ana
Redondo Angulo, Ibon
Villarroya i Gombau, Francesc
Keywords: Malalts cardíacs
Proteïnes
Cardiac patients
Proteins
Issue Date: 31-Aug-2015
Publisher: Frontiers Media
Abstract: The heart is not traditionally considered either a target or a site of fibroblast growth factor-21 (FGF21) production. However, recent findings indicate that FGF21 can act as a cardiomyokine; that is, it is produced by cardiac cells at significant levels and acts in an autocrine manner on the heart itself. The heart is sensitive to the effects of FGF21, both systemic and locally generated, owing to the expression in cardiomyocytes of β-Klotho, the key co-receptor known to confer specific responsiveness to FGF21 action. FGF21 has been demonstrated to protect against cardiac hypertrophy, cardiac inflammation, and oxidative stress. FGF21 expression in the heart is induced in response to cardiac insults, such as experimental cardiac hypertrophy and myocardial infarction in rodents, as well as in failing human hearts. Intracellular mechanisms involving PPARα and Sirt1 mediate transcriptional regulation of the FGF21 gene in response to exogenous stimuli. In humans, circulating FGF21 levels are elevated in coronary heart disease and atherosclerosis, and are associated with a higher risk of cardiovascular events in patients with type 2 diabetes. These findings provide new insights into the role of FGF21 in the heart and may offer potential therapeutic strategies for cardiac disease.
Note: Reproducció del document publicat a: https://doi.org/10.3389/fendo.2015.00133
It is part of: Frontiers In Endocrinology, 2015, vol. 6, p. 133
URI: http://hdl.handle.net/2445/138502
Related resource: https://doi.org/10.3389/fendo.2015.00133
ISSN: 1664-2392
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Files in This Item:
File Description SizeFormat 
655049.pdf1.87 MBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons