Abstract
We have recently demonstrated that aldehydic load contributes to the establishment/progression of myocardial infarction. Accumulation of 4-hydroxinonenal (4-HNE), a short and stable aldehyde generated during lipid peroxidation, results in protein-target inactivation and cardiac dysfunction. Aldehyde dehydrogenase 2 (ALDH2) plays a key role in metabolizing 4-HNE. Either pharmacological or …