通过抑制Pitx2,Nrf3介导的线粒体超氧化物促进心肌细胞亡并损害心脏功能
Qishan Chen1,2, Ancheng Zheng1,2, Xiaolei Xu1
1Department of Cardiology, Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, China (Q.C., A.Z., X.X., Z.S., M.Y., S.S., L.W., Y.W., L.Z.).
通过抑制Pitx2增加线粒体ROS和心肌细胞亡,核红素因子2相关因子3 (Nrf3) 加剧心肌梗塞 (MI). 抑制这种Nrf3-Pitx2通路可能为心脏病发作治疗提供新的治疗策略.
科学领域:
- 心脏病学
- 分子生物学
- 转氧化信号
背景情况:
- 心肌梗塞 (MI) 引发了线粒体反应性氧物种 (ROS) 和心肌细胞 (CM) 亡.
- 核红素因子2相关因子3 (Nrf3) 参与氧化还原信号传递和组织平衡.
研究的目的:
- 研究Nrf3在受伤后病态心脏重塑中的作用和机制.
- 评估Nrf3对CM亡和线粒体ROS产生的影响.
主要方法:
- 使用全球和CM特定的Nrf3淘汰小鼠接受MI.
- 用原发性心肌细胞和人类诱导的多能干细胞衍生的CM进行功能研究.
- 进行染色体免疫沉测序和免疫沉质谱测量以确定Nrf3标.
主要成果:
- 减少了线粒体ROS,CM亡和心脏重塑,改善了心脏功能.
- Nrf3通过增加Pitx2促进体的DNA甲基化来抑制Pitx2的表达.
- 而Pitx2过度表达减轻了MI引起的损伤.
结论:
- 通过抑制Pitx2增加线粒体ROS,Nrf3促进MI诱导的CM亡和心脏功能障碍.
- Nrf3-Pitx2-线粒体ROS轴是潜在的治疗点.
更多相关视频
07:14A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
07:40Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
相关概念视频
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
The Electron Transport Chain
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Mitochondrial Membranes
Electron Transport Chain: Complex III and IV
