| Literature DB >> 22507541 |
Dingxu Gong1, Hao Zhang, Shengshou Hu.
Abstract
Cardiac ischemia and reperfusion promote oxidative stress, leading to the accumulation of reactive aldehydes that cause cardiac damage. Mitochondrial aldehyde dehydrogenase 2 is emerging as a key cardioprotective enzyme for its central role in the detoxification of reactive aldehydes. Mitochondrial aldehyde dehydrogenase 2 activity strongly correlates to a better cardioprotective effect, and mitochondrial aldehyde dehydrogenase 2 can be activated by several pathways. After phosphorylation, the active mitochondrial aldehyde dehydrogenase 2 can reduce the build-up of aldehydes, inhibit autophagy, inhibit opening of the mitochondrial permeability transition pore, and prevent reperfusion arrhythmias. Therefore, mitochondrial aldehyde dehydrogenase 2 activation by small molecule activators suggests a promising new direction in cardiovascular research and the development of novel cardioprotective strategies. This review will discuss the cardioprotective effects of mitochondrial aldehyde dehydrogenase 2 activation in detail. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".Entities:
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Year: 2012 PMID: 22507541 DOI: 10.1016/j.yjmcc.2012.03.017
Source DB: PubMed Journal: J Mol Cell Cardiol ISSN: 0022-2828 Impact factor: 5.000