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中国临床研究英文版:2024,37(12):1928-1931
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铁死亡与炎症信号通路之间相互作用的研究进展
(昆明医科大学第二附属医院肾脏内科,云南 昆明 650000)
Research progress on the interaction between ferroptosis and inflammatory signaling pathway
(Department of Nephrology, The second affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650000, China)
摘要
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Received:November 03, 2023   Published Online:December 21, 2024
中文摘要: 铁死亡是一种由铁依赖的脂质过氧化、活性氧自由基大量积累所引起的细胞死亡方式,不同于细胞凋亡和其他方式的细胞死亡。炎症是机体对刺激的防御反应,表现为红、肿、热、痛和功能障碍,炎症反应的失衡会导致免疫系统紊乱、细胞功能障碍和死亡。越来越多的研究指出炎症的激活,包括多种炎症相关信号通路的激活,可导致铁死亡。在相关信号转导通路中,本综述重点关注了丝裂原激活蛋白激酶(MAPK)、核因子-κB(NF-κB)、Janus激酶信号转导和转录激活子(JAK/STAT)和环GMP-AMP合酶-干扰素基因刺激因子(cGAS-STING)这4条经典的炎症通路,并阐述了它们在铁死亡中的作用,讨论它们与铁死亡相关疾病发生的潜在机制,有助于进一步了解铁死亡的病理生理过程。
Abstract:Ferroptosis is a form of cell death characterized by iron-dependent lipid peroxidation and the accumulation of reactive oxygen species, distinct from apoptosis and other forms of cell death. Inflammation is the body’s defense response to stimuli, manifested as redness, swelling, heat, pain, and dysfunction, and an imbalance in the inflammatory response can lead to immune system dysregulation, cellular dysfunction, and death. Increasing researches suggest that the activation of inflammation, including the activation of various inflammation-related signaling pathways, can lead to ferroptosis. This review will focus on the classical inflammatory pathways, including the mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathways, and elucidate their roles in ferroptosis, discussing their potential mechanisms in the occurrence of diseases associated with ferroptosis, which contributes to a better understanding of the pathophysiological processes of ferroptosis.
文章编号:     中图分类号:R365    文献标志码:A
基金项目:国家自然科学基金地区科学基金项目(81860145);云南省中青年学术和技术带头人后备人才项目(202005AC160024);云南省科技厅应用基础研究项目(202001AT070008);兴滇英才支持计划(青年拔尖人才:YNWR-QNBJ-2020-269)
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