The role of TWEAK/Fn14 in cardiac remodeling

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...

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Veröffentlicht in:	Molecular biology reports 2012-11, Vol.39 (11), p.9971-9977
Hauptverfasser:	Ren, Man-Yi, Sui, Shu-Jian
Format:	Artikel
Sprache:	eng
Schlagworte:	Anatomy & physiology Animal Anatomy Animal Biochemistry Animals Apoptosis Apoptosis - physiology Biomedical and Life Sciences Cardiology Cardiomyopathy, Hypertrophic - metabolism Cell Proliferation Histology Humans Life Sciences Morphology Myocytes, Cardiac - cytology Myocytes, Cardiac - metabolism Pathology Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor - metabolism TWEAK Receptor Ventricular Remodeling - physiology
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Zusammenfassung:	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.
ISSN:	0301-4851 1573-4978
DOI:	10.1007/s11033-012-1867-6