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硫化氢作为心肌纤维化治疗的一种潜在替代方法。

Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis.

机构信息

Department of Oriental Medicine Biotechnology, College of Life Sciences, Kyung Hee University, Yongin 17104, Republic of Korea.

Department of Herbal Medicine Resource, Kangwon National University, Samcheok 25949, Republic of Korea.

出版信息

Oxid Med Cell Longev. 2020 Jan 23;2020:4105382. doi: 10.1155/2020/4105382. eCollection 2020.

DOI:10.1155/2020/4105382
PMID:32064023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6998763/
Abstract

Harmful, stressful conditions or events in the cardiovascular system result in cellular damage, inflammation, and fibrosis. Currently, there is no targeted therapy for myocardial fibrosis, which is highly associated with a large number of cardiovascular diseases and can lead to fatal heart failure. Hydrogen sulfide (HS) is an endogenous gasotransmitter similar to nitric oxide and carbon monoxide. HS is involved in the suppression of oxidative stress, inflammation, and cellular death in the cardiovascular system. The level of HS in the body can be boosted by stimulating its synthesis or supplying it exogenously with a simple HS donor with a rapid- or slow-releasing mode, an organosulfur compound, or a hybrid with known drugs (e.g., aspirin). Hypertension, myocardial infarction, and inflammation are exaggerated when HS is reduced. In addition, the exogenous delivery of HS mitigates myocardial fibrosis caused by various pathological conditions, such as a myocardial infarct, hypertension, diabetes, or excessive -adrenergic stimulation, via its involvement in a variety of signaling pathways. Numerous experimental findings suggest that HS may work as a potential alternative for the management of myocardial fibrosis. In this review, the antifibrosis role of HS is briefly addressed in order to gain insight into the development of novel strategies for the treatment of myocardial fibrosis.

摘要

心血管系统中有害的、有压力的条件或事件会导致细胞损伤、炎症和纤维化。目前,心肌纤维化尚无靶向治疗方法,而心肌纤维化与大量心血管疾病高度相关,并可导致致命性心力衰竭。硫化氢(HS)是一种内源性气体递质,类似于一氧化氮和一氧化碳。HS 参与抑制心血管系统中的氧化应激、炎症和细胞死亡。通过刺激其合成或用具有快速或缓慢释放模式的简单 HS 供体、有机硫化合物或与已知药物(如阿司匹林)的混合物来提高体内 HS 水平。当 HS 减少时,高血压、心肌梗死和炎症会被夸大。此外,通过参与多种信号通路,HS 的外源性传递减轻了由各种病理条件引起的心肌纤维化,如心肌梗死、高血压、糖尿病或过度 -肾上腺素能刺激。大量实验发现表明,HS 可能作为管理心肌纤维化的潜在替代方法。在这篇综述中,简要讨论了 HS 的抗纤维化作用,以便深入了解治疗心肌纤维化的新策略的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/6998763/b5bf862a76b6/OMCL2020-4105382.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/6998763/edf815ff684a/OMCL2020-4105382.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/6998763/b5bf862a76b6/OMCL2020-4105382.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/6998763/edf815ff684a/OMCL2020-4105382.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/6998763/b5bf862a76b6/OMCL2020-4105382.002.jpg

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