Key result
PRELP over-expression increased infarct size and interstitial fibrotic area and reduced cardiac function following acute myocardial infarction via the wnt/β-catenin signalling pathway.
Why the study?
Research was lacking on the role and underlying mechanism of PRELP in myocardial fibrosis and ventricular remodelling following acute myocardial infarction.
Does PRELP over-expression promote myocardial fibrosis and ventricular remodelling after acute myocardial infarction in preclinical models?
Does PRELP over-expression promote myocardial fibrosis and ventricular remodelling after acute myocardial infarction in preclinical models?
PRELP promotes myocardial fibrosis and ventricular remodeling after acute myocardial infarction via the wnt/β-catenin signaling pathway in preclinical models.
Answers are grounded in this paper and cite their sources.
PRELP overexpression promotes post-AMI fibrosis in models; leaves open its validation as a therapeutic target in humans.
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.
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Zhang et al. (2022) studied Acute myocardial infarction (n=60). PRELP over-expressing lentiviral vector / PRELP interference-expressed lentiviral vector vs. MI (myocardial infarction without PRELP modification) and SHAM was evaluated on Infarct size and interstitial fibrotic area. PRELP over-expression increased infarct size and interstitial fibrotic area and reduced cardiac function following acute myocardial infarction via the wnt/β-catenin signalling pathway.
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