State key Laboratory of Translational Cardiovascular Medicine, Fuwai Hospital & Cardiovascular Institute, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.
J Mol Cell Cardiol. 2013 Feb;55:58-63. doi: 10.1016/j.yjmcc.2012.03.017. Epub 2012 Apr 6.
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".
心肌缺血再灌注会促进氧化应激，导致活性醛类物质的积累，从而造成心脏损伤。线粒体乙醛脱氢酶 2 作为一种关键的心脏保护酶，因其在清除活性醛类物质方面的核心作用而备受关注。线粒体乙醛脱氢酶 2 的活性与更好的心脏保护效果密切相关，并且可以通过多种途径激活线粒体乙醛脱氢酶 2。磷酸化后，活性线粒体乙醛脱氢酶 2 可以减少醛类物质的积累，抑制自噬，抑制线粒体通透性转换孔的开放，并防止再灌注心律失常。因此，小分子激活剂激活线粒体乙醛脱氢酶 2 为心血管研究和新型心脏保护策略的发展提供了一个很有前途的新方向。本文将详细讨论线粒体乙醛脱氢酶 2 激活的心脏保护作用。本文是“关注心脏代谢特刊”的一部分。
