Atorvastatin treatment reduced fibrogenic activation of endocardial endothelial cells and increased KLF2 expression in in vitro and in vivo models of endocardial fibroelastosis.
Does atorvastatin reduce fibrogenic activation of endothelial cells in models of endocardial fibroelastosis?
Atorvastatin reduces fibrogenic activation of endocardial endothelial cells in preclinical models of endocardial fibroelastosis, suggesting a potential therapeutic role.
Endocardial fibroelastosis is a condition caused by the fibrogenic activation of endothelial cells via endothelial-to-mesenchymal transition of the endocardium, which is regulated by the transforming growth factor-β pathway. Atorvastatin, a statin, can protect the vascular endothelium by up-regulating KLF2 and inhibiting the transforming growth factor-β pathway. This study aimed to investigate the effects of atorvastatin on the fibrogenic activation of endothelial cells in the endocardium. The study found that atorvastatin treatment reduced fibrogenic activation of endocardial endothelial cells and increased KLF2 expression in both in vitro and in vivo models of endocardial fibroelastosis-related left ventricular restriction.
Diaz‐Gil et al. (Wed,) conducted a other in Endocardial fibroelastosis. Atorvastatin was evaluated on Fibrogenic activation of endocardial endothelial cells and KLF2 expression. Atorvastatin treatment reduced fibrogenic activation of endocardial endothelial cells and increased KLF2 expression in in vitro and in vivo models of endocardial fibroelastosis.