SRPX2 attenuated oxygen–glucose deprivation and reperfusion-induced injury in cardiomyocytes via alleviating endoplasmic reticulum stress-induced apoptosis through targeting PI3K/Akt/mTOR axis

Myocardial infraction (MI) is the leading cause of high morbidity and mortality worldwide. It was still urgently needed to find new and effective drugs for MI treatment by the use of myocardial ischemia/reperfusion (I/R) model. Sushi repeats contain the protein X-Linked 2 (SRPX2), which regulates a variety of important cell functions. However, its possible role in myocardial I/R and the progression of MI is still unclear. In this study, we investigated the role of SRPX2 in myocardial I/R. SRPX2 showed low expression in IR rats and H9C2 cells induced by oxygen–glucose deprivation/reperfusion (OGD/R). SRPX2 could increase OGD/R-induced H9C2 cell survival. In addition, SRPX2 suppressed the apoptosis of OGD/R-induced H9C2 cells. Furthermore, we found that SRPX2 could inhibit ER stress induced by OGD/R in H9C2 cells. Mechanically, we found that SRPX2 suppressed the PI3K/Akt/mTOR pathway, thus attenuating OGD/R -induced injury in H9C2 cells. Therefore, SRPX2 has the potential to serve as a target for MI treatment.