Why the study?
It was investigated whether electroacupuncture pretreatment alleviates myocardial injury by activating brown adipose tissue in acute myocardial infarction mice.
Does electroacupuncture pretreatment alleviate myocardial ischemia injury via brown adipose tissue activation in an AMI mouse model?
Does electroacupuncture pretreatment alleviate myocardial ischemia injury via brown adipose tissue activation in an AMI mouse model?
Electroacupuncture pretreatment at ST25 reduces myocardial ischemic injury in mice through the activation of brown adipose tissue and the BMP3b/Smad1/5 signaling pathway.
May reduce ischemic injury via BAT in AMI mice; leaves open clinical translation.
Acute myocardial infarction (AMI) is a critical condition that induces myocardial ischaemic injury and necrosis, requiring timely intervention to improve outcomes. Emerging evidence suggests that brown adipose tissue (BAT) plays a crucial role in cardiac protection by releasing bone morphogenetic protein 3b (BMP3b), which targets the Smad1/5 pathway in the heart. Here, we investigated whether Electroacupuncture (EA) pretreatment alleviates myocardial injury by activating BAT in AMI mice. The AMI model was established by left coronary artery ligation in male C57BL/6J mice, and EA was applied before AMI model establishment. Comprehensive assessments included morphological and molecular analyses of BAT, cardiac function evaluation, and infarct area measurements. The BMP3b/Smad1/5 signalling pathway was detected in BAT and the heart. Finally, we used mice with scapular BAT removed to verify the pivotal role of BAT in reducing myocardial injury caused by EA. The results showed that EA at ST25 enhanced BAT activation, upregulated BMP3b expression, promoted Smad1/5 phosphorylation, and increased the anti-apoptotic factor Bcl-xL, reducing myocardial damage. However, the protective effect of EA was not observed in the BAT-deficient mice. These findings suggest that EA at ST25 is a promising approach to reduce myocardial injury via the BAT and BMP3b/Smad1/5 pathways.
No takes yet. Share an insight, caveat, or question.
Yan et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: