ArticleCellular & molecular biology letters2026
Gut microbiota-derived trimethylamine N-oxide contributes to cardiomyocyte pyroptosis and cardiac injury via the tRF-Glu-ANT1-GSDMD axis.
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
aimsRecent research has shown that the gut microbiota arrests the progression of myocardial infarction (MI) by modulating immune inflammation, oxidative stress, and metabolism. However, the mechanism by which gut-derived trimethylamine N-oxide (TMAO) promotes cardiomyocyte pyroptosis following MI remains unclear. METHODS AND
resultsWe found that a high-choline diet exacerbated cardiac injury in mice by disrupting the intestinal barrier. Under high-choline conditions, the expression levels of tRF-1:31-Glu-TTC-2 (tRF-Glu) derived from tRF and tiRNAs (tsRNAs) were elevated, serving as a key target for intervention in cardiomyocyte pyroptosis. Loss of tRF-Glu significantly ameliorated TMAO-induced deterioration of myocardial fibrosis and cardiac function. Mechanistically, tRF-Glu directly binds to the mitochondrial inner membrane protein ANT1 and stabilizes its expression by inhibiting ubiquitination. Cardiomyocyte knockdown of ANT1 significantly blocked the generation of TMAO-induced cardiomyocyte mitochondrial reactive oxygen species, restored cardiomyocyte membrane potential, and reduced mitochondrial DNA (mtDNA) leakage.
conclusionsOur findings indicate that tRF-Glu inhibits the ubiquitination of ANT1 under the induction of TMAO, which in turn activates gasdermin D (GSDMD) and mtDNA release, accelerating cardiac remodeling. In conclusion, our study provides new insights into the role of the gut microbial metabolite-driven tRF-Glu–ANT1–GSDMD pathway in blocking cardiomyocyte pyroptosis and cardiac injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.