Pharmacological KLF-2 Upregulation Prevents Endocardial Fibroelastosis in an Animal Model of Congenital Heart Disease.

This article discusses the potential use of the lipophilic statin atorvastatin to prevent endocardial fibroelastosis (EFE) in congenital heart defects. EFE is regulated through the TGF-ß pathway via endothelial-to-mesenchymal transition (EndMT) in the endocardium. The study found that atorvastatin treatment reduced EndMT and increased the expression of the zing finger protein Krüppel-like factor 2 (KLF2), which protects the vascular endothelium. In an animal model, atorvastatin treatment resulted in a decrease in EFE thickness and myocardial infiltration. These findings suggest that upregulation of KLF2 with atorvastatin could be a potential treatment approach for patients with EFE. [Extracted from the article]