ArticleJournal of cardiovascular translational research2023
Eicosapentaenoic Acid Preserves Mitochondrial Quality and Attenuates Cardiac Remodeling After Myocardial Infarction in Rats.
Article in Journal of cardiovascular translational research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- Eicosapentaenoic acid ethyl ester, cardiac metabolomic and lipidomic signatures, and cardioprotection in myocardial infarction.European heart journal · 2026Article
- Identification of shared fatty acid metabolism related signatures in dilated cardiomyopathy and myocardial infarction.Future science OA · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eicosapentaenoic acid (EPA) reduces the risk of ischemic heart diseases and is a component of mitochondria. We herein investigated whether dietary EPA mediated mitochondrial fatty acid compositions, dynamics, and functions, resulting in the attenuation of cardiac remodeling after myocardial infarction (MI). The coronary artery of male rats was ligated to induce MI, and they were then treated with or without EPA (1000 mg/kg/day) for 12 weeks. The EPA treatment improved left ventricular systolic function and increased the mitochondrial content of EPA in the non-infarct region 12 weeks after MI. The content of ATP and mitochondrial complex II, III, and IV activities decreased after MI but were maintained by the EPA treatment in association with the preservation of optic atrophy 1, a mitochondrial fusion protein. The present results suggest that dietary EPA increased the mitochondrial content of EPA and preserved the expression of mitochondrial fusion proteins and energy metabolism, which attenuated left ventricular remodeling after MI.
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