ArticleWorld journal of experimental medicine2025
PI3K/AKT/GSK3β regulatory axis in bone mesenchymal stem cells initiates diabetic myocardial infarction
Article in World journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundWe aimed to identify the key proteins of miR-142-3p that regulate ferroptosis and ultimately control the downstream effectors of cardiomyocyte growth.
aimTo investigate the role of miR-142-3p in regulating ferroptosis and its impact on diabetes-induced myocardial infarction
methodsWe constructed bones mesenchymal stem cells (BMCs) with low miR-142-3p expression and investigated its role using cell flow cytometry and western blotting (WB). A diabetes myocardial infarction model was established using streptozotocin and coronary artery ligation. The rats were divided into six groups (
resultsWe observed that miR-142-3p increased BMC apoptosis and affected AKT and GSK3β. The myocardial infarction drug, liraglutide, BMCs, and miR-142-3p low expression BMCs intervention showed improvement in differing degrees. The liraglutide and BMCs showed significant blood glucose reduction (0.05). BMCs increased the expression of PI3K, AKT, and GSK3, leading to an increase in the myocardial infarction intervention group, liraglutide, and BMCs intervention groups. The low miR-142-3p expression intervention with BMCs group had the lowest PI3K and AKT protein expression. Liraglutide improved ferroptosis markers (increased COX-2, decreased GPX4 and CHCHD6). Low miR-142-3p BMCs increased COX-2, GPX4, and CHCHD6. CCM3 and VEGFR2 expression increased in BMCs and low miR-142-3p groups, promoting myocardial repair, but decreased in the low miR-142-3p groups.
conclusionThe preliminary results showed that the therapeutic mechanism of BMCs in diabetes myocardial infarction may involve miR-142-3p
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