ArticleNature communications2022
Gut microbiota production of trimethyl-5-aminovaleric acid reduces fatty acid oxidation and accelerates cardiac hypertrophy.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 97 citations in OpenAlex.
- Comparative insights into the gut-heart axis: cross-species and cross-population perspectives.Gut microbes · 2026Review
- Targeting of Pentraxin 3 Alleviated Cardiac Hypertrophy in Mice Induced by Angiotensin II.Clinical and experimental pharmacology & physiology · 2026Article
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- Structural Diversity and Analytical Characterization of Acylhomocarnitines.Journal of proteome research · 2026Article
- Glycoursodeoxycholic acid 3 sulfate sodium links hemodynamics and bile acid metabolism in aortic stenosis.Journal of advanced research · 2026Article
- Vegetarian Dietary Patterns and Diet-Related Metabolites Are Associated With Kidney Function in the Adventist Health Study-2 Cohort.Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation · 2026Article
- Metabolic syndrome and a broken heart: trust your gut or risk your heart.American journal of physiology. Heart and circulatory physiology · 2026Review
- Dietary metabolomic determinants of frailty through inflammation in the Canadian Longitudinal Study on Aging.npj aging · 2026Article
- Optical control of the cardiac rhythm with photoswitchable NaNature communications · 2026Article
- Tryptophan and polyamine metabolism dysregulation serves as an early marker of high-fat diet-induced glucose intolerance.Journal of lipid research · 2026Article
- The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026Review
- Role of Gut Microbiota in Diabetic HFpEF: Mechanisms and Therapeutic Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Prevention and Treatment of Doxorubicin and Trastuzumab-Induced Cardiotoxicity with Compound Danshen Dripping Pill.Chinese journal of integrative medicine · 2026Article
- Article
- Gut microbiota: new links between exercise and disease.Frontiers in microbiology · 2026Review
- The gut-heart axis in heart failure: from bidirectional pathophysiological mechanisms to integrative therapeutic strategies.Frontiers in microbiology · 2026Review
- Gut microbial metabolite connections to cardiovascular disease call for gutsy therapeutic approaches.The Journal of clinical investigation · 2025Article
- Decoding the impact of gut microbiota on heart failure.Genes & diseases · 2025Review
- Integration of localized microbiome, metabolome, and clinical datasets predicts healing in chronic wounds among veterans.bioRxiv : the preprint server for biology · 2025Article
- Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies found intestinal microbiota alterations which are thought to affect the development of various diseases through the production of gut-derived metabolites. However, the specific metabolites and their pathophysiological contribution to cardiac hypertrophy or heart failure progression still remain unclear. N,N,N-trimethyl-5-aminovaleric acid (TMAVA), derived from trimethyllysine through the gut microbiota, was elevated with gradually increased risk of cardiac mortality and transplantation in a prospective heart failure cohort (n = 1647). TMAVA treatment aggravated cardiac hypertrophy and dysfunction in high-fat diet-fed mice. Decreased fatty acid oxidation (FAO) is a hallmark of metabolic reprogramming in the diseased heart and contributes to impaired myocardial energetics and contractile dysfunction. Proteomics uncovered that TMAVA disturbed cardiac energy metabolism, leading to inhibition of FAO and myocardial lipid accumulation. TMAVA treatment altered mitochondrial ultrastructure, respiration and FAO and inhibited carnitine metabolism. Mice with γ-butyrobetaine hydroxylase (BBOX) deficiency displayed a similar cardiac hypertrophy phenotype, indicating that TMAVA functions through BBOX. Finally, exogenous carnitine supplementation reversed TMAVA induced cardiac hypertrophy. These data suggest that the gut microbiota-derived TMAVA is a key determinant for the development of cardiac hypertrophy through inhibition of carnitine synthesis and subsequent FAO.
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