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

IF 2.8 3区医学 Q3 ENDOCRINOLOGY & METABOLISM

Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy Pub Date : 2025-05-01 eCollection Date: 2025-01-01 DOI:10.2147/DMSO.S505138

Xiaoya Zhai, Yefei Gao, Haifei Lou, Liping Meng, Jiedong Zhou, Hui Lin, Fukang Xu

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Abstract

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 β-synthase (CBS), cystathionine γ-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.

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H2S在高糖诱导的心肌细胞和内皮细胞功能障碍中的保护作用：机制综述。

硫化氢（H2S）被认为是一种重要的气体递质，已被证明可以有效减少糖尿病对心肌细胞和内皮细胞造成的损伤。其保护作用主要源于多种机制，包括蛋白质的s -巯基化、减少细胞死亡、减轻线粒体损伤、改善离子通道功能障碍、与一氧化氮的相互作用以及调节血管生成。H2S由胱硫氨酸β-合成酶（CBS）、胱硫氨酸γ-裂解酶（CSE）和3-巯基丙酮酸硫转移酶（3-MST）合成，在糖尿病条件下，包括实验性高糖处理细胞和糖尿病动物模型中，其表达显著降低。本文总结了H2S及其供体在这些病理过程中的保护作用，强调了现有的研究空白，包括H2S供体靶向递送的挑战、有限的临床翻译和不完整的机制理解，并讨论了未来发展靶向H2S治疗策略的方向。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy Pharmacology, Toxicology and Pharmaceutics-Pharmacology

CiteScore

5.90

自引率

6.10%

发文量

431

审稿时长

16 weeks

期刊介绍： An international, peer-reviewed, open access, online journal. The journal is committed to the rapid publication of the latest laboratory and clinical findings in the fields of diabetes, metabolic syndrome and obesity research. Original research, review, case reports, hypothesis formation, expert opinion and commentaries are all considered for publication.