Key result
Forced expression of miR-24-3p alleviated cardiac fibrosis and suppressed mitophagy in transverse aortic constriction mice and Ang II-treated cardiac fibroblasts by downregulating PHB2.
Why the study?
Cardiac fibrosis is a pathological process leading to heart failure, and microRNAs play critical roles in regulating mitophagy and cardiac fibrosis.
Does increased expression of miR-24-3p alleviate cardiac fibrosis in TAC mice and Ang Ⅱ-treated cardiac fibroblasts?
Does increased expression of miR-24-3p alleviate cardiac fibrosis in TAC mice and Ang Ⅱ-treated cardiac fibroblasts?
Increased expression of miR-24-3p alleviates cardiac fibrosis by suppressing mitophagy via downregulation of PHB2, highlighting a potential therapeutic target for heart failure.
miR-24-3p may mitigate fibrosis in animal models; leaves open translation to human heart failure therapy.
Cardiac fibrosis is a pathological process of multiple cardiovascular diseases, which may lead to heart failure. Studies have shown that microRNAs (miRNAs) play critical roles in regulating mitophagy and cardiac fibrosis. We found that miR-24-3p expression was significantly downregulated in transverse aortic constriction (TAC) mice and cardiac fibroblasts (CFs) treated with Ang Ⅱ. We also found that, apart from improving cardiac structure and function, forced expression of miR-24-3p not only reduced the levels of collagen and α-SMA but also inhibited proliferation and migration of CFs. Next, our research proved that miR-24-3p suppressed the progression of mitophagy, autophagic flux, and the levels of mitophagy-related proteins in cardiac fibrosis models. Further analysis showed that PHB2 was a direct target of miR-24-3p. Finally, experiments showed that the knockdown of PHB2 reversed Ang Ⅱ-induced fibrosis in CFs. The results of our study suggests that increased expression of miR-24-3p contributes to the reduction of cardiac fibrosis and that it might be targeted therapeutically to alleviate cardiac fibrosis.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2022) studied Cardiac fibrosis. miR-24-3p was evaluated on Cardiac fibrosis and mitophagy progression. Forced expression of miR-24-3p alleviated cardiac fibrosis and suppressed mitophagy in transverse aortic constriction mice and Ang II-treated cardiac fibroblasts by downregulating PHB2.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: