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相关概念视频

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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The Electron Transport Chain01:30

The Electron Transport Chain

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The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
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Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Electron Transport Chain: Complex III and IV01:43

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During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...
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Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer
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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.).

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概括

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.

关键词:
细胞亡心肌细胞心肌梗塞反应性氧物种转录因子

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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.