Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission

Kensuke Tsushima; Heiko Bugger; Adam R. Wende; Jamie Soto; Gregory A. Jenson; Austin R. Tor; Rose McGlauflin; Helena Kenny; Yuan Zhang; Rhonda Souvenir; Xiao Xuan Hu; Crystal Sloan; Renata O. Pereira; Vitor A. Lira; Kenneth W. Spitzer; Terry L. Sharp; Kooresh I. Shoghi; Genevieve C. Sparagna; Eva A. Rog‐Zielinska; Peter Köhl; Oleh Khalimonchuk; Jean E. Schaffer; E. Dale Abel

doi:10.1161/circresaha.117.311307

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Abstract

Our results reveal a molecular mechanism by which lipid overload-induced mitochondrial ROS generation causes mitochondrial dysfunction by inducing post-translational modifications of mitochondrial proteins that regulate mitochondrial dynamics. These findings provide a novel mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy.

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Tsushima et al. (2017) studied this question.

synapsesocial.com/papers/69d93d8bccb0bba5a56847b9 https://doi.org/10.1161/circresaha.117.311307

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Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission

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Abstract

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Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission

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Abstract

Discussion

Cite This Study

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