Why the study?
Heart failure presents a major challenge, and emerging evidence indicates gut microbiota-derived trimethylamine N-oxide directly or indirectly mediates HF pathogenesis and serves as a prognostic marker, making it a potential therapeutic target.
This review highlights the role of the gut microbiota-derived metabolite TMAO in heart failure pathogenesis and its potential as a novel therapeutic target.
Should not yet change HF risk stratification or treatment; leaves open TMAO reduction as a therapeutic strategy.
Heart failure (HF) marks the culmination of numerous cardiac pathologies, presenting a major medical hurdle in prevention and treatment. In recent years, with the advancements in genomics and metabolomics, research has demonstrated that gut microbiota plays a significant role in the pathogenesis of HF. Trimethylamine N-oxide (TMAO) is a gut microbiota-derived metabolite and primarily sourced from foods abundant in choline, L-carnitine, and betaine. Research has shown that patients with HF exhibit higher levels of TMAO. Accumulating evidence has indicated that TMAO directly or indirectly mediates the occurrence and development of HF through multiple mechanisms. Furthermore, TMAO functions as a crucial prognostic marker in HF. Therefore, TMAO emerges as a potential therapeutic target for HF. This article reviews the generation and metabolic pathways of TMAO, emphasizes its pathophysiological mechanisms in HF, and explores promising therapeutic approaches targeting TMAO, offering novel insights and strategies for HF management.
No takes yet. Share an insight, caveat, or question.
Yu et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: