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硫化氢在不同疾病中调节铁死亡的作用。

The role of hydrogen sulfide regulation of ferroptosis in different diseases.

发表日期:2024 Jul 09
作者: Jingwen Lian, Yuhang Chen, Yanting Zhang, Shiyun Guo, Honggang Wang
来源: ANTIOXIDANTS & REDOX SIGNALING

摘要:

铁死亡是一种依赖铁和脂质过氧化的程序性细胞死亡。它不同于其他形式的程序性细胞死亡,如坏死、细胞凋亡和自噬。越来越多的证据表明铁死亡参与多种疾病,如神经退行性疾病、缺血再灌注损伤、心血管疾病等。因此,阐明铁死亡在疾病中的作用和机制对于进一步了解某些疾病的发病机制和治疗具有重要意义。硫化氢(H2S)是一种无色易燃气体,具有臭鸡蛋气味。许多年前,H2S 被认为是一种有毒气体。然而,近年来,越来越多的证据表明,它是继一氧化氮和一氧化碳之后第三种重要的气体信号分子。 H2S具有抗氧化应激、抗炎、抗凋亡、抗肿瘤等多种生理病理功能,可参与多种疾病的发生。据报道,H2S对铁死亡的调节在多种疾病中发挥着重要作用,但相关机制尚不完全清楚。在这篇综述中,我们回顾了近年来有关H2S调节铁死亡在疾病中的作用的文献,并分析了相关机制,希望为未来的深入研究提供参考。© 2024. The Author(s), under Exclusive License to Springer Science Business Media, LLC,隶属于 Springer Nature。
Ferroptosis is a programmed cell death that relies on iron and lipid peroxidation. It differs from other forms of programmed cell death such as necrosis, apoptosis and autophagy. More and more evidence indicates that ferroptosis participates in many types of diseases, such as neurodegenerative diseases, ischemia-reperfusion injury, cardiovascular diseases and so on. Hence, clarifying the role and mechanism of ferroptosis in diseases is of great significance for further understanding the pathogenesis and treatment of some diseases. Hydrogen sulfide (H2S) is a colorless and flammable gas with the smell of rotten eggs. Many years ago, H2S was considered as a toxic gas. however, in recent years, increasing evidence indicates that it is the third important gas signaling molecule after nitric oxide and carbon monoxide. H2S has various physiological and pathological functions such as antioxidant stress, anti-inflammatory, anti-apoptotic and anti-tumor, and can participate in various diseases. It has been reported that H2S regulation of ferroptosis plays an important role in many types of diseases, however, the related mechanisms are not fully clear. In this review, we reviewed the recent literature about the role of H2S regulation of ferroptosis in diseases, and analyzed the relevant mechanisms, hoping to provide references for future in-depth researches.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.