Conclusions
Our results showed that PRELP, through the wnt/β-catenin signalling pathway, led to myocardial fibrosis and ventricular remodelling following AMI.
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.