ArticleResearch (Washington, D.C.)2026
Astaxanthin Alleviates Intestinal Ferroptosis through Gut Commensal
Article in Research (Washington, D.C.), 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.
The trial behind it
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Authors and funding
10 authors.
Funding
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Abstract
Intestinal epithelial injury is increasingly linked to ferroptosis, yet how dietary bioactives engage the gut microbiota to restrain this process remains largely unresolved. Here, astaxanthin (ASTA) was identified as a microbiota-engaged regulator of intestinal ferroptosis and lipid peroxidation. ASTA markedly ameliorated dexamethasone-induced intestinal injury, and this protection was closely associated with the attenuation of epithelial ferroptosis. Depletion of the gut microbiota largely abolished the protective effect of ASTA, establishing the gut microbiota as an essential mediator of its intestinal bioactivity. Microbiome and metabolome profiling further revealed that ASTA reshaped the microbial metabolic landscape, with retinol metabolism emerging as a dominant pathway linked to ferroptosis resistance. Among the altered metabolites, retinoic acid was identified as a pivotal ASTA-associated metabolite that connected microbial remodeling with the restoration of epithelial anti-ferroptosis capacity. Metagenomics combined with in vitro bacterial metabolic assays identified
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Registered trials
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