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Gut Microbe-Generated Metabolite Trimethylamine-N-Oxide and Ischemic Stroke
1Department of Neurology, The First Affiliated Hospital of Soochow University, No. 899 Pinghai Road, Suzhou 215006, China.
Trimethylamine-N-oxide (TMAO), a metabolite linked to cardiovascular disease, is increasingly implicated in ischemic stroke development. This review explores TMAO
Area of Science:
- Cardiovascular Research
- Metabolomics
- Neurology
Background:
- Trimethylamine-N-oxide (TMAO) is a gut microbiota-derived metabolite.
- Elevated TMAO levels correlate with increased cardiovascular disease risk.
- Emerging evidence links TMAO to the pathogenesis of ischemic stroke.
Purpose of the Study:
- To review the relationship between TMAO and ischemic stroke risk factors, disease progression, and outcomes.
- To elucidate the mechanisms underlying TMAO's role in ischemic stroke.
- To evaluate interventions targeting the gut microbiota-TMAO pathway for stroke prevention and treatment.
Main Methods:
- Comprehensive literature review of preclinical and clinical studies.
- Analysis of TMAO's impact on atherosclerosis, thrombosis, and endothelial function.
- Evaluation of studies investigating gut microbiota modulation for TMAO reduction.
Main Results:
- TMAO promotes atherosclerosis and thrombosis via lipid metabolism, foam cell formation, and endothelial dysfunction.
- TMAO enhances platelet hyper-reactivity and vascular endothelial tissue factor activation.
- Mechanisms for TMAO's effect on stroke severity and recovery may involve inflammation and immune cell modulation.
Conclusions:
- TMAO is a significant factor in ischemic stroke development and progression.
- Targeting the gut microbiota-TMAO axis presents a promising therapeutic strategy for ischemic stroke.
- Further research is needed to clarify TMAO's precise role in stroke severity and neurological recovery.
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