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内源性硫化氢调控细胞凋亡:最新进展

Endogenous SO Controls Cell Apoptosis: The State-of-the-Art.

作者信息

Li Yingying, Feng Yingjun, Ye Xiaoyun, Peng Hanlin, Du Jiantong, Yao Xiaoli, Huang Yaqian, Jin Hongfang, Du Junbao

机构信息

Department of Pediatrics, Peking University First Hospital, Beijing, China.

Department of Cardiovascular Medicine, Children's Hospital Affiliated to Zhengzhou University/Children's Hospital of Henan Province, Zhengzhou, China.

出版信息

Front Cell Dev Biol. 2021 Oct 7;9:729728. doi: 10.3389/fcell.2021.729728. eCollection 2021.

Abstract

SO, previously known as the product of industrial waste, has recently been proven to be a novel gasotransmitter in the cardiovascular system. It is endogenously produced from the metabolism pathway of sulfur-containing amino acids in mammalians. Endogenous SO acts as an important controller in the regulation of many biological processes including cardiovascular physiological and pathophysiological events. Recently, the studies on the regulatory effect of endogenous SO on cell apoptosis and its pathophysiological significance have attracted great attention. Endogenous SO can regulate the apoptosis of vascular smooth muscle cells, endothelial cells, cardiomyocytes, neuron, alveolar macrophages, polymorphonuclear neutrophils and retinal photoreceptor cells, which might be involved in the pathogenesis of hypertension, pulmonary hypertension, myocardial injury, brain injury, acute lung injury, and retinal disease. Therefore, in the present study, we described the current findings on how endogenous SO is generated and metabolized, and we summarized its regulatory effects on cell apoptosis, underlying mechanisms, and pathophysiological relevance.

摘要

硫化氢(SO),以前被认为是工业废料的产物,最近已被证明是心血管系统中的一种新型气体信号分子。它在哺乳动物体内由含硫氨基酸的代谢途径内源性产生。内源性硫化氢在包括心血管生理和病理生理事件在内的许多生物过程的调节中起着重要的控制作用。最近,关于内源性硫化氢对细胞凋亡的调节作用及其病理生理意义的研究受到了极大关注。内源性硫化氢可以调节血管平滑肌细胞、内皮细胞、心肌细胞、神经元、肺泡巨噬细胞、多形核中性粒细胞和视网膜光感受器细胞的凋亡,这可能与高血压、肺动脉高压、心肌损伤、脑损伤、急性肺损伤和视网膜疾病的发病机制有关。因此,在本研究中,我们描述了内源性硫化氢如何产生和代谢的当前研究结果,并总结了其对细胞凋亡的调节作用、潜在机制和病理生理相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5431/8529009/c6fbbbacb5da/fcell-09-729728-g001.jpg

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