ArticleiScience2026
Butyrate ameliorates doxorubicin-induced heart failure by inhibiting cardiomyocyte ferroptosis through the gut-heart axis.
Article in iScience, 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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8 authors.
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Abstract
Doxorubicin (DOX), a widely used chemotherapeutic agent, is clinically limited by DOX-induced heart failure (DIHF). Emerging evidence links gut microbial dysbiosis to exacerbating DIHF progression, yet the mechanisms remain elusive. Herein, we established a rat DIHF susceptibility model to investigate the gut microbiota's regulatory role. Multi-omics analyses indicated that DIHF severity was associated with reduced butyrate-producing bacteria and systemic butyrate levels. Sodium butyrate (NaB) significantly alleviated DOX-induced cardiomyocyte toxicity and DIHF. Mechanistically, NaB strengthened the colonic and cardiac barrier functions and reduced gut microbiota translocation to the heart and cardiac lipopolysaccharide (LPS) accumulation. NaB altered cardiac bacterial composition and functions, reduced cardiac Fe
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