The protective role of brown adipose tissue in cardiac cell damage after myocardial infarction and heart failure
Xu Z., Li H., Cao G., Li P., Zhou H., Sun Y.
Narrative Review on Cardiovascular Disease, published in Lipids Health Dis (2024) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Lipids Health Dis (2024)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 39415186
- PMCID
- PMC11481725
- DOI
- 10.1186/s12944-024-02326-3
- Citations
- 6
Abstract (original English)
Acute myocardial infarction (AMI) and related cardiovascular disease complications are the leading causes of mortality worldwide. Brown adipose tissue (BAT) is thermogenic and characterized by the uncoupling protein expression. Recent studies have found that in cardiovascular diseases, activated BAT can effectively improve the prognosis of AMI and concurrent heart failure through intercellular communication. However, a clear and systematic understanding of the myocardial protective mechanism of BAT after AMI is lacking, especially in the endocrine function of BAT. This review describes the effects of BAT on various cells in the heart after AMI. BAT plays a protective role on cardiac cells and fibroblasts during ischemia/reperfusion (I/R), myocardial remodeling, and myocardial fibrosis. This review also discusses the changes caused by BAT activation in different stages of heart failure. Finally, this review summarizes the treatment methods that target BAT to improve AMI. Further in-depth researches are still needed to clarify the underlying mechanism of the connection between BAT and different cells in cardiac tissue in order to identify potential therapeutic targets.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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