Hydrogen sulfide mitigates mitochondrial dysfunction and cellular senescence in diabetic patients: Potential therapeutic applications

IF 5.3 2区医学 Q1 PHARMACOLOGY & PHARMACY Biochemical pharmacology Pub Date : 2024-09-25 DOI:10.1016/j.bcp.2024.116556

Ting Chen , Dacheng Bai , Changyong Gong , Yu Cao , Xiaoqing Yan , Renyi Peng

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Abstract

Diabetes induces a pro-aging state characterized by an increased abundance of senescent cells in various tissues, heightened chronic inflammation, reduced substance and energy metabolism, and a significant increase in intracellular reactive oxygen species (ROS) levels. This condition leads to mitochondrial dysfunction, including elevated oxidative stress, the accumulation of mitochondrial DNA (mtDNA) damage, mitophagy defects, dysregulation of mitochondrial dynamics, and abnormal energy metabolism. These dysfunctions result in intracellular calcium ion (Ca²⁺) homeostasis disorders, telomere shortening, immune cell damage, and exacerbated inflammation, accelerating the aging of diabetic cells or tissues. Hydrogen sulfide (H₂S), a novel gaseous signaling molecule, plays a crucial role in maintaining mitochondrial function and mitigating the aging process in diabetic cells. This article systematically explores the specific mechanisms by which H₂S regulates diabetes-induced mitochondrial dysfunction to delay cellular senescence, offering a promising new strategy for improving diabetes and its complications.

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硫化氢可减轻糖尿病患者的线粒体功能障碍和细胞衰老：潜在的治疗应用。

糖尿病会诱发一种促衰老状态，其特征是各种组织中衰老细胞的数量增加、慢性炎症加剧、物质和能量代谢降低以及细胞内活性氧（ROS）水平显著增加。这种情况会导致线粒体功能障碍，包括氧化应激升高、线粒体 DNA（mtDNA）损伤积累、有丝分裂缺陷、线粒体动力学失调和能量代谢异常。这些功能障碍会导致细胞内钙离子（Ca2+）平衡失调、端粒缩短、免疫细胞损伤和炎症加剧，从而加速糖尿病细胞或组织的衰老。硫化氢（H2S）是一种新型气体信号分子，在维持线粒体功能和缓解糖尿病细胞衰老过程中发挥着至关重要的作用。本文系统地探讨了 H2S 调节糖尿病诱导的线粒体功能障碍以延缓细胞衰老的具体机制，为改善糖尿病及其并发症提供了一种前景广阔的新策略。

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来源期刊

Biochemical pharmacology 医学-药学

CiteScore

10.30

自引率

1.70%

发文量

420

审稿时长

17 days

期刊介绍： Biochemical Pharmacology publishes original research findings, Commentaries and review articles related to the elucidation of cellular and tissue function(s) at the biochemical and molecular levels, the modification of cellular phenotype(s) by genetic, transcriptional/translational or drug/compound-induced modifications, as well as the pharmacodynamics and pharmacokinetics of xenobiotics and drugs, the latter including both small molecules and biologics. The journal''s target audience includes scientists engaged in the identification and study of the mechanisms of action of xenobiotics, biologics and drugs and in the drug discovery and development process. All areas of cellular biology and cellular, tissue/organ and whole animal pharmacology fall within the scope of the journal. Drug classes covered include anti-infectives, anti-inflammatory agents, chemotherapeutics, cardiovascular, endocrinological, immunological, metabolic, neurological and psychiatric drugs, as well as research on drug metabolism and kinetics. While medicinal chemistry is a topic of complimentary interest, manuscripts in this area must contain sufficient biological data to characterize pharmacologically the compounds reported. Submissions describing work focused predominately on chemical synthesis and molecular modeling will not be considered for review. While particular emphasis is placed on reporting the results of molecular and biochemical studies, research involving the use of tissue and animal models of human pathophysiology and toxicology is of interest to the extent that it helps define drug mechanisms of action, safety and efficacy.