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Mitochondrial Dynamics in Cardiovascular Medicine pp 265–276Cite as

Mechanistic Role of Thioredoxin 2 in Heart Failure

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 982))

Abstract

Thioredoxin 2 (Trx2) is a pivotal mitochondrial protein that regulates redox signaling. The mitochondrial Trx2 is expressed ubiquitously, but it is found at the highest levels in metabolically active tissues like the heart. Global gene knockout of Trx2 results in embryonic lethality, likely due to the increased cellular oxidative stress. Moreover, mice with cardiac-specific Trx2 deletion develop spontaneous dilated cardiomyopathy (DCM), correlating with increased apoptosis stress kinase-1 (ASK1) signaling and increased cardiomyocyte apoptosis. Cardiomyocyte apoptosis is a common mechanism in the pathogenesis of heart failure. Our results show that Trx2 is essential for maintaining cardiac function. In this chapter, we summarize the key mechanistic role of Trx2 in preserving cardiac function by suppressing mitochondrial reactive oxygen species (ROS) generation and by inhibiting ASK1-dependent apoptosis in heart failure. Trx2 and ASK1 represent promising targets to develop therapeutic strategies for the treatment of DCM and heart failure.

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    Authors and Affiliations

    1. The First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou, China

      Chaofei Chen, Haixuan Chen, Weidong Ji & Wang Min

    2. Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St, 401B, New Haven, CT, 06520, USA

      Huanjiao Jenny Zhou & Wang Min

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    1. Dept. of Biomedical Advanced Sciences, Federico II University, Naples, Italy

      Gaetano Santulli

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    Chen, C., Chen, H., Zhou, H.J., Ji, W., Min, W. (2017). Mechanistic Role of Thioredoxin 2 in Heart Failure. In: Santulli, G. (eds) Mitochondrial Dynamics in Cardiovascular Medicine. Advances in Experimental Medicine and Biology, vol 982. Springer, Cham. https://doi.org/10.1007/978-3-319-55330-6_14

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