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Reviews of Physiology, Biochemistry and Pharmacology Vol. 170 pp 101–127Cite as

Cardiac Response to Oxidative Stress Induced by Mitochondrial Dysfunction

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Part of the book series: Reviews of Physiology, Biochemistry and Pharmacology ((REVIEWS,volume 170))

Abstract

The heart works without resting, requiring enormous amounts of energy to continuously pump blood throughout the body. Because of its considerable energy requirements, the heart is vulnerable to oxidative stress caused by the generation of endogenous reactive oxygen species (ROS). Therefore, the heart has effective regulatory and adaptive mechanisms to protect against oxidative stress. Inherited or acquired mitochondrial respiratory chain dysfunction disrupts energy metabolism and causes excessive ROS production and oxidative stress. The physiological cardiac response to oxidative stress can strengthen the heart, but pathological cardiac responses or altered regulatory mechanisms can cause heart disease. Therefore, mitochondria-targeted antioxidants have been tested and some are used clinically. In this review, we briefly discuss the role of mitochondrial DNA mutations, mitochondrial dysfunction, and ROS generation in the development of heart disease and recent developments in mitochondria-targeted antioxidants for the treatment of heart disease.

Conflict of interest: None.

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Acknowledgments

This study was supported by a grant from the Priority Research Centers Program and Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education, Science and Technology (2010–0020224, 2012R1A2A1A03007595, 2012R1A1A2005240, and 2011–0028925), Republic of Korea.

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  1. Department of Physiology, Department of Health Sciences and Technology, National Research Laboratory for Mitochondrial Signaling, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan, South Korea

    Hyoung Kyu Kim, Nari Kim, Kyung Soo Ko, Byoung Doo Rhee & Jin Han

  2. Department Cell Molecular Medicine, Laboratory Ion Channel Research, Campus Gasthuisberg, KU Leuven, Leuven, Belgium

    Bernd Nilius

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  1. Hyoung Kyu Kim
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  6. Jin Han
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Correspondence to Jin Han .

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  1. KU Leuven, Leuven, Belgium

    Bernd Nilius

  2. Cardiovascular Research Center, Loyola University Chicago, Maywood, Illinois, USA

    Pieter de Tombe

  3. Walther-Straub-Institut für Pharmakologi, München, Germany

    Thomas Gudermann

  4. Department of Neurobiology, Max-Planck-Institute, Göttingen, Germany

    Reinhard Jahn

  5. Department of Cytobiology, University of Marburg, Marburg, Germany

    Roland Lill

  6. Cardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom

    Ole H. Petersen

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Kim, H.K., Nilius, B., Kim, N., Ko, K.S., Rhee, B.D., Han, J. (2016). Cardiac Response to Oxidative Stress Induced by Mitochondrial Dysfunction. In: Nilius, B., de Tombe, P., Gudermann, T., Jahn, R., Lill, R., Petersen, O. (eds) Reviews of Physiology, Biochemistry and Pharmacology Vol. 170. Reviews of Physiology, Biochemistry and Pharmacology, vol 170. Springer, Cham. https://doi.org/10.1007/112_2015_5004

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