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- W2406403848 endingPage "44" @default.
- W2406403848 startingPage "535" @default.
- W2406403848 abstract "Acute myocardial infarction is one of the major causes of mortality worldwide. Reperfusion in a timely fashion is the most effective way to limit infarct size. However, reperfusion can itself prompt further myocardial injury. This phenomenon is commonly known as myocardial ischemia-reperfusion (IR) injury. Mitochondrial aldehyde dehydrogenase (ALDH2) is an enzyme metabolizing acetaldehyde and toxic aldehydes. Increasing evidence has revealed a cardioprotective role of ALDH2 in myocardial IR injury. Evidence from animal studies has shown that ALDH2 diminishes acute myocardial infarct size, ameliorates cardiac dysfunction and prevents reperfusion arrhythmias. The activity of ALDH2 is severely compromised if it is encoded by the mutant ALDH2*2 gene, with an incidence of approximately 40% in Asian populations. Epidemiological surveys in the Asian population have depicted that ALDH2 polymorphism is closely associated with higher prevalence of acute myocardial infarction and coronary artery disease. Therefore, targeting ALDH2 may represent a promising avenue to protect against IR injury. This review recapitulates the underlying mechanisms involved in the protective effect of ALDH2 in cardiac IR injury. Translational potential of ALDH2 in the management of coronary heart disease is also discussed." @default.
- W2406403848 created "2016-06-24" @default.
- W2406403848 creator A5015937552 @default.
- W2406403848 creator A5032451475 @default.
- W2406403848 creator A5042332666 @default.
- W2406403848 creator A5072447321 @default.
- W2406403848 date "2015-12-25" @default.
- W2406403848 modified "2023-09-23" @default.
- W2406403848 title "Mitochondrial aldehyde dehydrogenase in myocardial ischemia-reperfusion injury: from bench to bedside." @default.
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- W2406403848 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26701629" @default.
- W2406403848 hasPublicationYear "2015" @default.
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