ArticleJournal of physiology and biochemistry2025
PLAC8 as a potential therapeutic target for myocardial infarction: unraveling the molecular mechanisms.
Article in Journal of physiology and biochemistry, 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
The incidence of myocardial infarction (MI) has been increasing in recent years, and the cause of acute myocardial infarction is apoptosis due to insufficient coronary myocardial blood supply. PLAC8 is a critical gene in the disease process of MI through GEO database research and analysis of differentially expressed genes (DEGs). In this study, in mice with myocardial infarction caused by surgical ligation of the left anterior descending coronary artery (LAD) and hypoxia-induced H9C2 cells as a model, the myocardium of the model group was found to show severe cardiomyocyte disorders, apoptosis of inflammatory cell infiltration, and ischemic state by HE, TTC, and Tunel staining. The expression of PLAC8 was reduced in the disease model by PCR and Western blot, and the expression of cle-Casp3 and Bax was also found to be high. However, overexpression of PLAC8 in the disease model reversed these processes. MEK/ERK and P65 are the core signaling pathways in the MI model. In this study, we found that the therapeutic effect of PLAC8 was related to the inhibition of the MEK/ERK signaling pathway by overexpression of PLAC8 and antagonism of the MEK/ERK signaling pathway. In conclusion, the inhibition of the MEK/ERK signaling pathway by PLAC8 under hypoxic conditions reduces apoptosis in H9c2 cells, which may provide new ideas for the determination and treatment of MI.
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