ArticleApoptosis : an international journal on programmed cell death2023
Upregulation of miR-29b-3p alleviates coronary microembolization-induced myocardial injury via regulating BMF and GSK-3β.
Article in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Molecular mechanisms of coronary microembolization-induced MINOCA.Basic research in cardiology · 2026Review
- EV-transferred miR-7111-3p inhibits malignant phenotypes and tumor growth in nasopharyngeal carcinoma via targeting APP-regulated epithelial-mesenchymal transition.Journal of translational medicine · 2026Article
- Thioredoxin system dysregulation and calpain activation drive myocardial disulfidptosis via pathological disulfide bonds remodeling.Cell death discovery · 2026Article
- Semaglutide ameliorates coronary microembolization-induced injury by suppressing apoptosis and inflammation via the HMGB1/RAGE/NF-κB p65 pathway.Journal of geriatric cardiology : JGC · 2026Article
- Association between circulating levels of miR-29 and postoperative neurological complications in acute type A aortic dissection patients.Frontiers in cardiovascular medicine · 2026Article
- Bcl-2 modifying factor (Bmf): "a mysterious stranger" in the Bcl-2 family proteins.Cell death and differentiation · 2026Review
- HMGB1 regulates autophagy via TLR4/NF-κB signaling pathway in myocardial injury induced by coronary microembolization.European journal of medical research · 2025Article
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary microembolization (CME) is an intractable complication results from acute coronary syndrome. CME-induced myocardial apoptosis was associated with progressive cardiac contractile dysfunction. miR-29b-3p has been reported implicated in variety cardiovascular diseases, but its function in CME-induced myocardial injury is yet unknown. Herein, a rat model of CME was established by injecting microspheres into the left ventricle and found that the expression level of miR-29b-3p was markedly decreased in the CME rat heart tissues. By using echocardiography, CD31 immunohistochemistry staining, hematoxylin basic fuchsin picric acid (HBFP) staining, TUNEL staining, and western blotting analysis after CME, it was found that upregulating miR-29b-3p improved cardiac dysfunction, promoted angiogenesis, decreased myocardial microinfarct area, and inhibited myocardial apoptosis. Additionally, miR-29b-3p inhibition can reverse the protective benefits of miR-29b-3p overexpression. Mechanistically, the target genes of miR-29b-3p were identified as glycogen synthase kinase 3 (GSK-3β) and Bcl-2 modifying factor (BMF) by bioinformatics analysis and luciferase reporter experiment. Overall, our findings imply that induction of miR-29b-3p, which negatively regulates GSK-3β and BMF expression, attenuates CME-induced myocardial injury, suggesting a novel potential therapeutic target for cardioprotective after CME.
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