ArticleCardiovascular journal of Africa
PRELP promotes myocardial fibrosis and ventricular remodelling after acute myocardial infarction by the wnt/β-catenin signalling pathway.
Article in Cardiovascular journal of Africa. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026Review
- Mouse digit AAV gene delivery into fibroblasts regulates regenerative outcome.Science advances · 2026Article
- Prognostic utility of Wnt/β-catenin signaling pathway biomarkers in predicting outcomes of patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Wnt Signaling Inhibitors as Therapeutic Approach in Ischemic Heart Disease.Molecules (Basel, Switzerland) · 2024Review
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Article
- Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention.Frontiers in pharmacology · 2023Review
- The role of β-catenin in cardiac diseases.Frontiers in pharmacology · 2023Review
- Integrated analysis of WGCNA and machine learning identified diagnostic biomarkers in dilated cardiomyopathy with heart failure.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesProline/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.
methodsIn this study, we established AMI mouse and cellculture models in an oxygen-glucose deprivation environment.
resultsWe 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.
conclusionsOur results showed that PRELP, through the wnt/β-catenin signalling pathway, led to myocardial fibrosis and ventricular remodelling following AMI.
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