title: The role of TWEAK/Fn14 in cardiac remodeling.
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.
authors: Department of Cardiology, Shandong Provincial Chest Hospital, Jinan 250013, China.
authors: Man-Yi
authors: MY
authors: Ren
authors: Shu-Jian
authors: SJ
authors: Sui
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002312:Cardiomyopathy, Hypertrophic / Q000378:metabolism; D049109:Cell Proliferation; D006801:Humans; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000378:metabolism*; D000074050:TWEAK Receptor; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D018124:Receptors, Tumor Necrosis Factor; C000613297:TNFRSF12A protein, human; D000074050:TWEAK Receptor