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内源性二氧化硫:心血管系统中气体信号分子家族的新成员。

Endogenous Sulfur Dioxide: A New Member of Gasotransmitter Family in the Cardiovascular System.

作者信息

Huang Yaqian, Tang Chaoshu, Du Junbao, Jin Hongfang

机构信息

Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.

Department of Physiology and Pathophysiology, Peking University Health Science Centre, Beijing 100191, China; Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China.

出版信息

Oxid Med Cell Longev. 2016;2016:8961951. doi: 10.1155/2016/8961951. Epub 2015 Dec 29.

DOI:10.1155/2016/8961951
PMID:26839635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4709694/
Abstract

Sulfur dioxide (SO2) was previously regarded as a toxic gas in atmospheric pollutants. But it has been found to be endogenously generated from metabolism of sulfur-containing amino acids in mammals through transamination by aspartate aminotransferase (AAT). SO2 could be produced in cardiovascular tissues catalyzed by its synthase AAT. In recent years, studies revealed that SO2 had physiological effects on the cardiovascular system, including vasorelaxation and cardiac function regulation. In addition, the pathophysiological effects of SO2 were also determined. For example, SO2 ameliorated systemic hypertension and pulmonary hypertension, prevented the development of atherosclerosis, and protected against myocardial ischemia-reperfusion (I/R) injury and isoproterenol-induced myocardial injury. These findings suggested that endogenous SO2 was a novel gasotransmitter in the cardiovascular system and provided a new therapy target for cardiovascular diseases.

摘要

二氧化硫(SO₂)曾被视为大气污染物中的一种有毒气体。但现已发现,在哺乳动物体内,含硫氨基酸通过天冬氨酸转氨酶(AAT)转氨作用进行代谢可内源性生成SO₂。在其合酶AAT的催化下,心血管组织中也可产生SO₂。近年来,研究表明SO₂对心血管系统具有生理作用,包括血管舒张和心脏功能调节。此外,还确定了SO₂的病理生理作用。例如,SO₂可改善系统性高血压和肺动脉高压,预防动脉粥样硬化的发展,并保护心肌免受缺血再灌注(I/R)损伤和异丙肾上腺素诱导的心肌损伤。这些发现表明内源性SO₂是心血管系统中的一种新型气体信号分子,为心血管疾病提供了新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e9/4709694/a7660b146911/OMCL2016-8961951.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e9/4709694/a7660b146911/OMCL2016-8961951.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e9/4709694/a7660b146911/OMCL2016-8961951.001.jpg

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