Protective Role of H2S in High Glucose-Induced Cardiomyocyte and Endothelial Cell Dysfunction: A Mechanistic Review

被引：0

作者：

Zhai, Xiaoya ^{[1
]}

Gao, Yefei ^{[1
]}

Lou, Haifei ^{[1
]}

Meng, Liping ^{[1
]}

Zhou, Jiedong ^{[2
]}

Lin, Hui ^{[3
]}

Xu, Fukang ^{[1
]}

机构：

[1] Shaoxing Peoples Hosp, Dept Cardiol, Shaoxing, Peoples R China

[2] Ningbo Univ, Cardiovasc Med, Affiliated Hosp 1, Ningbo 315211, Zhejiang, Peoples R China

[3] Ningbo Univ, Affiliated Lihuili Hosp, Dept Cardiol, Hlth Sci Ctr, Ningbo 315211, Zhejiang, Peoples R China

来源：

DIABETES METABOLIC SYNDROME AND OBESITY | 2025年 / 18卷

关键词：

H2S; diabetic cardiomyopathy; diabetes-induced endothelial cell damage; EXOGENOUS HYDROGEN-SULFIDE; INDUCED INJURY; NITRIC-OXIDE; INDUCED APOPTOSIS; S-SULFHYDRATION; SULFANE SULFUR; METABOLISM; MITOCHONDRIA; PATHWAY; RAT;

D O I：

10.2147/DMSO.S505138

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hydrogen sulfide (H2S), recognized as a significant gasotransmitter, has been shown to effectively reduce damage to cardiomyocytes and endothelial cells caused by diabetes. Its protective effects primarily stem from several mechanisms, including S-sulfhydration of proteins, reduction of cell death, alleviation of mitochondrial damage, improvement of ion channel dysfunction, interaction with nitric oxide, and modulation of angiogenesis. H2S is synthesized by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST), whose expression is significantly reduced under diabetic conditions, including experimental high-glucose treatment in cells and diabetes mellitus animal models. This review summarizes the protective role of H2S and its donors in these pathological processes, highlights existing research gaps-including challenges in the targeted delivery of H2S donors, limited clinical translation, and incomplete mechanistic understanding-and discusses future directions for developing targeted H2S-based therapeutic strategies.

引用

页码：1373 / 1388

页数：16

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