ArticleAnimal models and experimental medicine2026
Establishment of a mouse model of TMAO-induced cardiac injury and application of MICT intervention.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Gut Microbiota in Metabolic Syndrome: Differences in Microbial Signatures and Clinical Profiles.Medicina (Kaunas, Lithuania) · 2026Review
- Establishment of a mouse model of TMAO-induced cardiac injury and application of MICT intervention.Animal models and experimental medicine · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundThis study aims to explore the establishment of an animal model of cardiac injury induced by trimethylamine-N-oxide (TMAO), a metabolite secreted by gut microorganisms, and to investigate its application in moderate-intensity continuous training (MICT) intervention.
methodsC57BL6/J mice were randomly divided into four groups: normal mice (Nor, n = 15); mice administered TMAO (TMAO, n = 15); mice undergoing (Nor+MICT, n = 15); mice undergoing (MICT) and administered TMAO (TMAO+MICT, n = 15). Mice in the TMAO and TMAO+MICT groups received daily gavage of high-dose TMAO for 8 weeks, whereas those in the Nor+MICT and TMAO+MICT groups underwent MICT for 8 weeks (60 min per session, 5 days per week, at 50% maximal running capacity). Cardiac function was evaluated using ultrasound, myocardial histology was examined using hematoxylin and eosin (HE) staining, and nuclear magnetic resonance (NMR)-based metabolomics was employed for multivariate statistical and metabolic pathway analyses.
resultsRelative to the Nor group, TMAO-treated mice exhibited significant weight loss, elevated heart rate, and reduced ejection fraction and left ventricular fractional shortening, indicating cardiac impairment. Importantly, the TMAO+MICT group demonstrated significant improvements in these parameters compared to the TMAO group, alongside distinct alterations in myocardial metabolic profiles. TMAO altered five metabolic pathways relative to controls, whereas MICT induced significant changes in three pathways in TMAO-treated mice.
conclusionEight weeks of high-dose TMAO administration induced significant cardiac dysfunction in mice, which was effectively mitigated by MICT intervention. Consequently, this animal model serves as a valuable tool for investigating the mechanisms underlying the impact of MICT on cardiovascular diseases.
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