ArticleScientific reports2022
Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Percentage of Low-Attenuation Epicardial Adipose Volume (LAAV%) as an Independent Predictor of Coronary Microvascular Dysfunction: A Retrospective Cohort Study.Reviews in cardiovascular medicine · 2026Article
- PCPE-1 promotes cardiac fibrosis with aging and obesity.JCI insight · 2026Article
- [Mechanisms of gutZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- MiR-499-5P/PACS2/TRPV1 Axis Maintains Mitochondrial Homeostasis and Left Ventricular Function after Extreme Cold Stress.Journal of cardiovascular translational research · 2026Article
- Itaconate Promotes Cold Adaptation and Myocardial Protection by Enhancing Brown Adipose Tissue Metabolism.Metabolites · 2026Article
- A Cross-Layer Inflammatory Signature Links Residual Inflammatory Risk to Heart Failure Risk in Metabolic Syndrome: Network Mapping and Brown Adipose Transcriptomic Support.Journal of inflammation research · 2026Article
- Gut-derived metabolites and mitochondrial homeostasis in heart failure: mechanistic links and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Combined aerobic and resistance exercise training restores perivascular adipose tissue function in the thoracic aorta of rats with heart failure.Clinical science (London, England : 1979) · 2025Article
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- Cellular and Molecular Mechanisms Explaining the Link Between Inflammatory Bowel Disease and Heart Failure.Cells · 2025Review
- Gut-heart axis: cardiac remodeling and heart failure in the context of inflammatory bowel disease and dysbiosis.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Microbiota, mitochondria, and epigenetics in health and disease: converging pathways to solve the puzzle.Pflugers Archiv : European journal of physiology · 2025Review
- Therapeutic potential of ketone bodies on exercise intolerance in heart failure: looking beyond the heart.Cardiovascular research · 2025Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Cold exposure and the cardiovascular system: from physiological adaptation to pathological risk.Frontiers in physiology · 2025Review
- The protective role of brown adipose tissue in cardiac cell damage after myocardial infarction and heart failure.Lipids in health and disease · 2024Review
- Low-Molecular-Weight Compounds Produced by the Intestinal Microbiota and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Gut Microbiota-Derived Trimethylamine Promotes Inflammation with a Potential Impact on Epigenetic and Mitochondrial Homeostasis in Caco-2 Cells.Antioxidants (Basel, Switzerland) · 2024Article
- UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
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Authors and funding
31 authors at 13 institutions in 3 countries.
Funding
Abstract
Low body temperature predicts a poor outcome in patients with heart failure, but the underlying pathological mechanisms and implications are largely unknown. Brown adipose tissue (BAT) was initially characterised as a thermogenic organ, and recent studies have suggested it plays a crucial role in maintaining systemic metabolic health. While these reports suggest a potential link between BAT and heart failure, the potential role of BAT dysfunction in heart failure has not been investigated. Here, we demonstrate that alteration of BAT function contributes to development of heart failure through disorientation in choline metabolism. Thoracic aortic constriction (TAC) or myocardial infarction (MI) reduced the thermogenic capacity of BAT in mice, leading to significant reduction of body temperature with cold exposure. BAT became hypoxic with TAC or MI, and hypoxic stress induced apoptosis of brown adipocytes. Enhancement of BAT function improved thermogenesis and cardiac function in TAC mice. Conversely, systolic function was impaired in a mouse model of genetic BAT dysfunction, in association with a low survival rate after TAC. Metabolomic analysis showed that reduced BAT thermogenesis was associated with elevation of plasma trimethylamine N-oxide (TMAO) levels. Administration of TMAO to mice led to significant reduction of phosphocreatine and ATP levels in cardiac tissue via suppression of mitochondrial complex IV activity. Genetic or pharmacological inhibition of flavin-containing monooxygenase reduced the plasma TMAO level in mice, and improved cardiac dysfunction in animals with left ventricular pressure overload. In patients with dilated cardiomyopathy, body temperature was low along with elevation of plasma choline and TMAO levels. These results suggest that maintenance of BAT homeostasis and reducing TMAO production could be potential next-generation therapies for heart failure.
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