ArticleFrontiers in cardiovascular medicine2026
Empagliflozin attenuates elaidic acid-exacerbated cardiac dysfunction post-myocardial infarction via suppression of the NF-κB/NLRP3 pathway.
Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Myocardial infarction leads to heart failure greatly increasing the risk of adverse cardiovascular events. Empagliflozin (EMPA), a sodium-dependent glucose transporters 2 (SGLT2) inhibitor, has been demonstrated to provide effective cardiovascular protection, while the underlying metabolic mechanisms of EMPA on protecting cardiac dysfunction post-MI remain incompletely clear. The current study was conducted to investigate the metabolic effects of EMPA in hearts with cardiac dysfunction post-MI. Methods: Bioinformatics analysis revealed activation of the NF-κB/NLRP3/pyroptosis signaling pathway in AMI patients. Results: The bioinformatics analysis was conducted using GSE97320 dataset found the activation of the NF-κB/NLRP3/pyroptosis signaling pathway in MI patients. Conclusion: EMPA treatment effectively improves cardiac structure and function in MI mice, potentially through regulating lipid metabolism and reducing tissue EA levels, thereby inhibiting NF-κB/NLRP3/pyroptosis while alleviating mitochondrial structural and functional abnormalities.
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