过度表达UCP2激活SIRT3,以调节由心肌损伤引起的氧化应激和线粒体动态

Zhengguang Geng1, Wenbo Chen2, Qinju Lu2

  • 1Department of Critical Care Medicine, Affiliated hospital of Zunyi Medical University, Zunyi, Guizhou, 563000, China; Guizhou Key Laboratory of Anesthesia and Organ Protection& Zunyi Medical University, Zunyi, Guizhou, 563000, China.

概括

脱蛋白-2 (UCP2) 的过度表达通过减少氧化应激和稳定线粒体,可以防止心肌缺血-再输液损伤. 赛尔图因-3 (SIRT3) 参与了这种保护机制.

相关概念视频

The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
4.6K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
2.4K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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...
13.4K