Objectives: Proline/arginine-rich end leucine-rich repeat protein (PRELP) has been reported to contribute to the remodelling of cardiovascular tissues in the ischaemia-reperfusion injury model. However, research is lacking on the role of PRELP in myocardial fibrosis and ventricular remodelling, and the mechanism through which PRELP brings about these changes is not clear. This study aimed to evaluate the role of PRELP in ventricular remodelling and myocardial fibrosis following acute myocardial infarction (AMI) and to explore the underlying mechanism.
Methods: In this study, we established AMI mouse and cellculture models in an oxygen-glucose deprivation environment.
Results: We found that over-expression of PRELP increased the infarct size and interstitial fibrotic area. Expression of the wnt/β-catenin pathway molecules, which are downstream of PRELP, increased more in the PRELP over-expression group than in the AMI group.
Conclusions: Our results showed that PRELP, through the wnt/β-catenin signalling pathway, led to myocardial fibrosis and ventricular remodelling following AMI.
Keywords: PRELP; acute myocardial infarction; myocardial fibrosis; wnt; β‐catenin.