发病机制
串扰
心力衰竭
射血分数保留的心力衰竭
医学
心脏病学
内科学
机制(生物学)
细胞外
射血分数
自噬
内分泌学
化学
细胞内
心脏功能不全
病态的
作者
Q Pan,Cheng Chen,Ce Zhang,Yao Jiang,Ziqin Zhou,Han Zhang,Thomas G. Gillette,Joseph A Hill,Gabriele G. Schiattarella,Guixin Wu,Yuejin Yang,GuiHao Chen
摘要
The present work unveils a mechanism whereby obesity promotes HFpEF progression, emphasizing the role of VAT-heart crosstalk. Specifically, VAT-derived sEVs, miR-295-3p, and the resultant disruption of cardiac autophagy contribute significantly to the pathogenesis of HFpEF.
科研通智能强力驱动
Strongly Powered by AbleSci AI