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Recent advances in the protective role of hydrogen sulfide in myocardial ischemia/reperfusion injury: a narrative review.近年来硫化氢在心肌缺血/再灌注损伤保护作用的研究进展:一篇综述。
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2
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Zofenopril Protects Against Myocardial Ischemia-Reperfusion Injury by Increasing Nitric Oxide and Hydrogen Sulfide Bioavailability.佐芬普利通过提高一氧化氮和硫化氢的生物利用度来预防心肌缺血再灌注损伤。
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本文引用的文献

1
The role of mitochondrial reactive oxygen species, NO and H S in ischaemia/reperfusion injury and cardioprotection.线粒体活性氧、NO 和 H₂S 在缺血/再灌注损伤及心脏保护中的作用。
J Cell Mol Med. 2020 Jun;24(12):6510-6522. doi: 10.1111/jcmm.15279. Epub 2020 May 8.
2
Inhibition of TGFβ-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression.抑制 TGFβ 激活的蛋白激酶 1 通过抑制内质网应激改善心肌缺血/再灌注损伤。
J Cell Mol Med. 2020 Jun;24(12):6846-6859. doi: 10.1111/jcmm.15340. Epub 2020 May 7.
3
Bisoprolol, a β antagonist, protects myocardial cells from ischemia-reperfusion injury via PI3K/AKT/GSK3β pathway.比索洛尔,一种β受体拮抗剂,通过PI3K/AKT/GSK3β信号通路保护心肌细胞免受缺血再灌注损伤。
Fundam Clin Pharmacol. 2020 Dec;34(6):708-720. doi: 10.1111/fcp.12562. Epub 2020 May 25.
4
LncRNA GOLGA2P10 is induced by PERK/ATF4/CHOP signaling and protects tumor cells from ER stress-induced apoptosis by regulating Bcl-2 family members.长链非编码 RNA GOLGA2P10 由 PERK/ATF4/CHOP 信号诱导产生,并通过调节 Bcl-2 家族成员来保护肿瘤细胞免受 ER 应激诱导的细胞凋亡。
Cell Death Dis. 2020 Apr 24;11(4):276. doi: 10.1038/s41419-020-2469-1.
5
Dose-Dependent Effects of Long-Term Administration of Hydrogen Sulfide on Myocardial Ischemia-Reperfusion Injury in Male Wistar Rats: Modulation of RKIP, NF-κB, and Oxidative Stress.长期给予硫化氢对雄性 Wistar 大鼠心肌缺血再灌注损伤的剂量依赖性影响:RKIP、NF-κB 和氧化应激的调节。
Int J Mol Sci. 2020 Feb 19;21(4):1415. doi: 10.3390/ijms21041415.
6
Hydrogen Sulfide Switch Phenomenon Regulating Autophagy in Cardiovascular Diseases.硫化氢开关现象调控心血管疾病自噬。
Cardiovasc Drugs Ther. 2020 Feb;34(1):113-121. doi: 10.1007/s10557-019-06927-4.
7
Effect of gasotransmitters treatment on expression of hypertension, vascular and cardiac remodeling and hypertensive nephropathy genes in left ventricular hypertrophy.气体信号分子处理对左心室肥厚中高血压、血管和心脏重构及高血压肾病基因表达的影响。
Gene. 2020 May 5;737:144479. doi: 10.1016/j.gene.2020.144479. Epub 2020 Feb 14.
8
The protective effects of hydrogen sulfide on the myocardial ischemia via regulating Bmal1.硫化氢通过调节 Bmal1 对心肌缺血的保护作用。
Biomed Pharmacother. 2019 Dec;120:109540. doi: 10.1016/j.biopha.2019.109540. Epub 2019 Oct 19.
9
HS Protects against Cardiac Cell Hypertrophy through Regulation of Selenoproteins.HS 通过调节硒蛋白来防止心肌细胞肥大。
Oxid Med Cell Longev. 2019 Sep 10;2019:6494306. doi: 10.1155/2019/6494306. eCollection 2019.
10
CaMKII mediates myocardial ischemia/reperfusion injury‑induced contracture in isolated rat heart.钙调蛋白激酶II介导离体大鼠心脏中由心肌缺血/再灌注损伤引起的挛缩。
Mol Med Rep. 2019 Aug 1. doi: 10.3892/mmr.2019.10550.

近年来硫化氢在心肌缺血/再灌注损伤保护作用的研究进展:一篇综述。

Recent advances in the protective role of hydrogen sulfide in myocardial ischemia/reperfusion injury: a narrative review.

机构信息

Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.

Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.

出版信息

Med Gas Res. 2021 Apr-Jun;11(2):83-87. doi: 10.4103/2045-9912.311499.

DOI:10.4103/2045-9912.311499
PMID:33818448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8130667/
Abstract

Hydrogen sulfide (HS) is recognized to be a novel mediator after carbon monoxide and nitric oxide in the organism. It can be produced in various mammalian tissues and exert many physiological effects in many systems including the cardiovascular system. A great amount of recent studies have demonstrated that endogenous HS and exogenous HS-releasing compounds (such as NaHS, NaS, and GYY4137) provide protection in many cardiovascular diseases, such as ischemia/reperfusion injury, heart failure, cardiac hypertrophy, and atherosclerosis. In recent years, many mechanisms have been proposed and verified the protective role exhibited by HS against myocardial ischemia/reperfusion injury, and this review is to demonstrate the protective role of exogenous and endogenous HS on myocardial ischemia/reperfusion injury.

摘要

硫化氢(HS)是继一氧化碳和一氧化氮之后在体内被发现的一种新型介质。它可以在各种哺乳动物组织中产生,并在包括心血管系统在内的许多系统中发挥许多生理作用。大量最近的研究表明,内源性 HS 和外源性 HS 释放化合物(如 NaHS、NaS 和 GYY4137)在许多心血管疾病中提供保护,如缺血/再灌注损伤、心力衰竭、心肌肥厚和动脉粥样硬化。近年来,许多机制被提出并验证了 HS 对心肌缺血/再灌注损伤的保护作用,本综述旨在展示外源性和内源性 HS 对心肌缺血/再灌注损伤的保护作用。