| Literature DB >> 22752727 |
Abstract
The pathophysiological basis of heart failure is cardiac remodeling, a process that comprises structural and functional changes including cardiomyocyte proliferation, hypertrophy, necrosis, apoptosis, autophagy, interstitial fibrosis, contractile dysfunction and ventricular dilatation. Accumulating evidence demonstrate that tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is involved in the process by binding its receptor fibroblast growth factor-inducible molecule 14 (Fn14). In this review, we will discuss the potential role of the TWEAK/Fn14 axis in cardiac remodeling, elucidate its possible mechanisms and explore new therapeutic targets for heart failure.Entities:
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Year: 2012 PMID: 22752727 DOI: 10.1007/s11033-012-1867-6
Source DB: PubMed Journal: Mol Biol Rep ISSN: 0301-4851 Impact factor: 2.316