ArticleBiology2026
Metformin Attenuates Sepsis-Induced Cardiomyopathy via Inhibition of Reverse Electron Transfer at Mitochondrial Complex I.
Article in Biology, 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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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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10 authors.
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Abstract
Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication of sepsis; however, its molecular mechanisms remain incompletely understood, which has hindered the development of targeted therapies. We hypothesized that excessive mitochondrial reactive oxygen species (mtROS) production through reverse electron transfer (RET) at mitochondrial complex I contributes to septic myocardial injury and that metformin, a clinically used inhibitor of mitochondrial complex I, protects the myocardium by inhibiting this process. In lipopolysaccharide-stimulated H9C2 cardiomyocytes and cecal ligation and puncture-induced septic rats, sepsis was characterized by an elevated mitochondrial membrane potential, accompanied by succinate accumulation, an increased NADH/NAD
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