Journal
MOLECULAR BIOLOGY REPORTS
Volume 39, Issue 11, Pages 9971-9977Publisher
SPRINGER
DOI: 10.1007/s11033-012-1867-6
Keywords
TWEAK; Fn14; Cardiac remodeling; Signaling pathway
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Funding
- Key Technologies R&D Program of Shandong Province [2007GG10002014]
- Natural Science Foundation of Shandong Province [Y2007C073]
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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.
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