The abstract describes a study designed to evaluate whether oral eicosapentaenoic acid attenuates cardiac remodeling after myocardial infarction, but no results are reported.
Does oral eicosapentaenoic acid (EPA) improve mitochondrial fatty acid composition, dynamics, and oxidative phosphorylation to attenuate cardiac remodeling after myocardial infarction?
Myocardial infarction (MI) model
Oral eicosapentaenoic acid (EPA)
Mitochondrial fatty acid composition, dynamics, oxidative phosphorylation, and attenuation of cardiac remodelingsurrogate
This study aims to investigate the mechanistic role of oral EPA on mitochondrial dynamics and oxidative phosphorylation in attenuating cardiac remodeling after myocardial infarction.
Purpose: Eicosapentaenoic acid (EPA) is a first line drug in the management after myocardial infarction. Mitochondria are major contributors to energy metabolism and recent mounting evidence suggests that mitochondrial dynamics, such as fusion and fission, has a pivotal role in regulating mitochondrial function. This study was designed to determine whether oral EPA mediates mitochondrial fatty acid composition, dynamics, and oxidative phosphorylation, leading to the attenuation of cardiac remodeling after myocardial infarction (MI).
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Kobara et al. (Fri,) conducted a other in myocardial infarction. oral Eicosapentaenoic acid (EPA) was evaluated on mitochondrial fatty acid composition, dynamics, and oxidative phosphorylation. The abstract describes a study designed to evaluate whether oral eicosapentaenoic acid attenuates cardiac remodeling after myocardial infarction, but no results are reported.
www.synapsesocial.com/papers/69f027214a030179bdc8d748 — DOI: https://doi.org/10.1093/eurheartj/eht308.p1857
Miyuki Kobara
Takuya Shiraishi
Kazuki Noda
European Heart Journal
Kyoto Pharmaceutical University
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