Fibroblast-derived miR-425-5p alleviates cardiac remodelling in heart failure via inhibiting the TGF-β1/Smad signalling.

ABSTRACT: The pathological activation of cardiac fibroblasts (CFs) plays a crucial role in the development of pressure overload-induced cardiac remodelling and subsequent heart failure (HF). Growing evidence demonstrates that multiple microRNAs (miRNAs) are abnormally expressed in the pathophysiologic process of cardiovascular diseases, with miR-425 recently reported to be potentially involved in HF. In this study, we aimed to investigate the effects of fibroblast-derived miR-425-5p in pressure overload-induced HF and explore the underlying mechanisms. C57BL/6 mice were injected with a recombinant adeno-associated virus specifically designed to overexpress miR-425-5p in CFs, followed by transverse aortic constriction (TAC) surgery. Neonatal mouse CFs (NMCFs) were transfected with miR-425-5p mimics a

SUBMITTER: Zhou H 

PROVIDER: S-EPMC11552651 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature