Scholarlink

Abstract <p>Cardiovascular diseases (CVDs) threaten the human health. Lots of researches suggest that ROS accumulates in cardiomyocytes in CVDs. Excessive mitochondrial autophagy caused by reactive oxygen species (ROS) impairs the function of cardiomyocytes. Here, we found that extracellular vesicles derived human umbilical cord blood plasma (UCB-EV) inhibited oxidative stress-induced mitophagy to promote cell survival. The viability of UCB-EV pre-protected H9C2 cardiomyocytes was maintained after H<sub>2</sub>O<sub>2</sub> exposure. In addition, UCB-EV partially restored mitochondrial membrane potential and promoted mitochondrial biogenesis. Furthermore, PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine protein kinase, was inhibited by UCB-EV during oxidative stress. We further demonstrate the role of UCB-EV in inhibiting mitophagy to make H9C2 cells survival by PINK1/Parkin pathway. Our findings elucidate the protective mechanism of UCB-EV against oxidative stress in H9C2 cells. These findings reveal the potential role of UCB-EV in alleviate oxidative stress in cardiomyocytes.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Extracellular Vesicles Derived from Human Umbilical Cord Blood Plasma Protect H2O2-Induced Oxidative Damage by Inhibiting Mitophagy in H9C2 Cells

  • 期刊论文

  • 发表日期：

    2025年6月10日

查看全文
  • Yi Jiang,
  • Haoyang Zhou,
  • Rong Cheng,
  • Yanan Pu,
  • Di Wang,
  • Yangyang Jiao,
  • Xinyu Li,
  • Yan Chen

摘要

Abstract

Cardiovascular diseases (CVDs) threaten the human health. Lots of researches suggest that ROS accumulates in cardiomyocytes in CVDs. Excessive mitochondrial autophagy caused by reactive oxygen species (ROS) impairs the function of cardiomyocytes. Here, we found that extracellular vesicles derived human umbilical cord blood plasma (UCB-EV) inhibited oxidative stress-induced mitophagy to promote cell survival. The viability of UCB-EV pre-protected H9C2 cardiomyocytes was maintained after H2O2 exposure. In addition, UCB-EV partially restored mitochondrial membrane potential and promoted mitochondrial biogenesis. Furthermore, PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine protein kinase, was inhibited by UCB-EV during oxidative stress. We further demonstrate the role of UCB-EV in inhibiting mitophagy to make H9C2 cells survival by PINK1/Parkin pathway. Our findings elucidate the protective mechanism of UCB-EV against oxidative stress in H9C2 cells. These findings reveal the potential role of UCB-EV in alleviate oxidative stress in cardiomyocytes.