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外源性硫化氢通过调节自噬在缺血/再灌注损伤中发挥重要作用。

Exogenous Hydrogen Sulfide Plays an Important Role Through Regulating Autophagy in Ischemia/Reperfusion Injury.

作者信息

Lv Shuangyu, Wang Zhu, Wang Jie, Wang Honggang

机构信息

Henan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, China.

Henan Technician College of Medicine and Health, Kaifeng, China.

出版信息

Front Mol Biosci. 2021 May 13;8:681676. doi: 10.3389/fmolb.2021.681676. eCollection 2021.

DOI:10.3389/fmolb.2021.681676
PMID:34055892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8155623/
Abstract

Ischemia/reperfusion (I/R) injury is characterized by limiting blood supply to organs, then restoring blood flow and reoxygenation. It leads to many diseases, including acute kidney injury, myocardial infarction, circulatory arrest, ischemic stroke, trauma, and sickle cell disease. Autophagy is an important and conserved cellular pathway, in which cells transfer the cytoplasmic contents to lysosomes for degradation. It plays an important role in maintaining the balance of cell synthesis, decomposition and reuse, and participates in a variety of physiological and pathological processes. Hydrogen sulfide (HS), along with carbon monoxide (CO) and nitric oxide (NO), is an important gas signal molecule and regulates various physiological and pathological processes. In recent years, there are many studies on the improvement of I/R injury by HS through regulating autophagy, but the related mechanisms are not completely clear. Therefore, we summarize the related research in the above aspects to provide theoretical reference for future in-depth research.

摘要

缺血/再灌注(I/R)损伤的特点是限制器官的血液供应,然后恢复血流和再氧合。它会导致许多疾病,包括急性肾损伤、心肌梗死、循环骤停、缺血性中风、创伤和镰状细胞病。自噬是一种重要且保守的细胞途径,细胞通过该途径将细胞质内容物转移到溶酶体进行降解。它在维持细胞合成、分解和再利用的平衡中起重要作用,并参与多种生理和病理过程。硫化氢(HS)与一氧化碳(CO)和一氧化氮(NO)一样,是一种重要的气体信号分子,可调节各种生理和病理过程。近年来,有许多关于HS通过调节自噬改善I/R损伤的研究,但相关机制尚不完全清楚。因此,我们总结了上述方面的相关研究,为未来的深入研究提供理论参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c602/8155623/cbcf9a25b21b/fmolb-08-681676-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c602/8155623/cbcf9a25b21b/fmolb-08-681676-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c602/8155623/cbcf9a25b21b/fmolb-08-681676-g001.jpg

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