Emerging relationship between hydrogen sulfide and ferroptosis: A literature review

IF 1.4 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Acta biochimica Polonica Pub Date : 2023-12-07 DOI:10.18388/abp.2020_6756
Xiaoming Gao, Ke Lu, Chong Li
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Abstract

Gaseous hydrogen sulfide (H2S) can function as a signaling molecule similar to nitric oxide or carbon monoxide under physiological conditions, ultimately exerting anti-inflammatory, anti-apoptotic, and antioxidant activities. Many studies have investigated the role of H2S in a variety of biological contexts, and both endogenous H2S and H2S donors have been leveraged as tools for fundamental biomedical research, and it has been suggested that they may provide value for the design of novel therapeutic strategies in the years to come. Ferroptotic cell death is a distinct programmed cell death resulting from excessive lipid peroxidation in an iron-dependent manner, and is characterized by high levels of iron accumulation, reactive oxygen species (ROS) production, and peroxidation of cellular lipids. Several recent studies have revealed a close relationship between ferroproteins and their precursors, H2S, and the enzymes that produce them. This review summarizes the current information pertaining to the relationship between ferroptosis and H2S, with a particular focus on the underlying mechanisms and biological applications of this knowledge.
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硫化氢与铁中毒之间的新关系:文献综述
气态硫化氢(H2S)在生理条件下可以作为一种类似一氧化氮或一氧化碳的信号分子,最终发挥抗炎、抗凋亡和抗氧化活性。许多研究已经调查了H2S在各种生物环境中的作用,并且内源性H2S和H2S供体都被用作基础生物医学研究的工具,并且有人认为它们可能在未来几年为设计新的治疗策略提供价值。嗜铁性细胞死亡是一种独特的程序性细胞死亡,由铁依赖方式引起的过度脂质过氧化引起,其特征是高水平的铁积累、活性氧(ROS)的产生和细胞脂质过氧化。最近的几项研究揭示了铁蛋白与其前体H2S以及产生它们的酶之间的密切关系。本文综述了目前有关铁下垂与H2S之间关系的信息,特别关注这一知识的潜在机制和生物学应用。
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
Acta biochimica Polonica
Acta biochimica Polonica 生物-生化与分子生物学
CiteScore
2.40
自引率
0.00%
发文量
99
审稿时长
4-8 weeks
期刊介绍: Acta Biochimica Polonica is a journal covering enzymology and metabolism, membranes and bioenergetics, gene structure and expression, protein, nucleic acid and carbohydrate structure and metabolism.
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