Magea13 attenuates myocardial injury in acute myocardial infarction by inhibiting the cAMP-PKA signaling pathway

ObjectAcute myocardial infarction (AMI) is a serious cardiovascular disease for which there are still no effective therapeutic options available, and melanoma-associated antigen-A13 (Magea13), a member of the MAGE superfamily, has an unknown role in AMI. This study aims to investigate the potential role and molecular mechanisms of Magea13 in myocardial injury associated with AMI through in vivo and in vitro experiments.MethodsFirstly, differentially expressed genes (DEGs) and signaling pathways were screened by RNA sequencing. Cardiac-specific Magea13 overexpression was achieved with the adeno-associated virus type 9 serotype system. Subsequently, these rats underwent left anterior descending coronary artery (LAD) ligation, followed by histopathological examination, biochemical assay, and Western blot analysis to evaluate the efficacy and feasibility of Magea13 in AMI. Meanwhile, the Magea13-overexpressing rat cardiomyocyte cell line (H9c2) was also subjected to hypoxia-glucose deficiency/reperfusion to mimic AMI injury to further validate its effects in vitro.ResultsThe cardiomyocyte-specific overexpression of Magea13 was observed to attenuate myocardial injury in rats with acute myocardial infarction. Furthermore, Magea13 overexpression was demonstrated to attenuate OGD/R-induced H9c2 cell injury. Mechanistic studies have suggested that the protective effect of Magea13 may be mediated through the cAMP-PKA pathway.ConclusionMagea13 has been demonstrated to offer protection against AMI myocardial injury through the cAMP-PKA signaling pathway and is therefore a promising therapeutic and predictive target for AMI myocardial injury.