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IDH2 deficiency promotes mitochondrial dysfunction and cardiac hypertrophy in mice

Authors
Ku, Hyeong JunAhn, YoungkeunLee, Jin HyupPark, Kwon MooPark, Jeen-Woo
Issue Date
3월-2015
Publisher
ELSEVIER SCIENCE INC
Keywords
IDH2; Redox status; Cardiac hypertrophy; Apoptosis; Mitochondria
Citation
FREE RADICAL BIOLOGY AND MEDICINE, v.80, pp.84 - 92
Indexed
SCIE
SCOPUS
Journal Title
FREE RADICAL BIOLOGY AND MEDICINE
Volume
80
Start Page
84
End Page
92
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/94253
DOI
10.1016/j.freeradbiomed.2014.12.018
ISSN
0891-5849
Abstract
Cardiac hypertrophy, a risk factor for heart failure, is associated with enhanced oxidative stress in the mitochondria, resulting from high levels of reactive oxygen species (ROS). The balance between ROS generation and ROS detoxification dictates ROS levels. As such, disruption of these processes results in either increased or decreased levels of ROS. In previous publications, we have demonstrated that one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDH2) is to control the mitochondrial redox balance, and-thereby mediate the cellular defense against oxidative damage, via the production of NADPH. To explore the association between IDH2 expression and cardiac function, we measured myocardial hypertrophy, apoptosis, and contractile dysfunction in IDH2 knockout (idh2(-/-)) and wild-type (idh2(+/+)) mice. As expected, mitochondria from the hearts of knockout mice lacked IDH2 activity and the hearts of IDH2-deficient mice developed accelerated heart failure, increased levels of apoptosis and hypertrophy, and exhibited mitochondrial dysfunction, which was associated with a loss of redox homeostasis. Our results suggest that IDH2 plays an important role in maintaining both baseline mitochondrial function and cardiac contractile function following pressure-overload hypertrophy, by preventing oxidative stress. (C) 2014 Elsevier Inc. All rights reserved.
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