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The role of TWEAK/Fn14 in cardiac remodeling

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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.

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Acknowledgments

This work was supported by grants from the Key Technologies R&D Program of Shandong Province (grant number 2007GG10002014) and the Natural Science Foundation of Shandong Province (Y2007C073).

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None declared.

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  1. Department of Cardiology, Shandong Provincial Chest Hospital, 46 Lishan Road, Jinan, 250013, China

    Man-Yi Ren

  2. Department of Cardiology, Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, China

    Shu-Jian Sui

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  1. Man-Yi Ren
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Correspondence to Shu-Jian Sui.

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Ren, MY., Sui, SJ. The role of TWEAK/Fn14 in cardiac remodeling. Mol Biol Rep 39, 9971–9977 (2012). https://doi.org/10.1007/s11033-012-1867-6

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