Functional analysis reveals heart failure-related regulation of apoptosis and fibrosis by miR-150-5p, suggesting a therapeutic target for treatment.
MiR-150-5p is a microRNA that plays an important role in the heart diseases. However, its specific role and molecular mechanism in heart failure (HF) remain unclear. In this study, we found that miR-150-5p was downregulated in patients with HF, while the expression of MMP14 was elevated. In vitro experiments have shown that miR-150-5p directly targets MMP14 and inhibits its expression in human aortic smooth muscle cells (HASMCs). Functionally, miR-150-5p promotes the proliferation, migration and apoptosis of HASMC, which is a key process in the progression of HF. In the HF mouse model induced by transverse aortic contraction (TAC), overexpression of miR-150-5p can improve cardiac function, reduce hypertrophy and fibrosis, while its inhibition aggravates these effects. These findings determined that miR-150-5p is a protective regulator in HF, functioning by inhibiting MMP14, and indicated its potential as a therapeutic target for HF treatment.
No takes yet. Share an insight, caveat, or question.
Yu et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: