ArticleAdipocyte2025
Electroacupuncture pretreatment alleviates myocardial ischemia injury via brown adipose tissue and BMP3b/Smad1/5 pathway in mice.
Article in Adipocyte, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.