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解析微囊藻毒素-LR在铁死亡和脓毒症发病机制中的作用:综述

Unraveling the Role of Microcystin-LR in Ferroptosis and Sepsis Pathogenesis: A Comprehensive Review.

作者信息

Ying Honglian, Zhao Hongli, Zhang Xiaqiu, Feng Haoyuan, Zhou Manjuan, Wu Zunqiu, Wu Ning

机构信息

Chemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang 550025, China.

出版信息

Biomolecules. 2025 Jun 30;15(7):947. doi: 10.3390/biom15070947.

DOI:10.3390/biom15070947
PMID:40723819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12292872/
Abstract

Sepsis, a systemic inflammatory response syndrome triggered by infection, is characterized by acute onset, rapid progression, and high mortality. Ferroptosis, a form of programmed cell death induced by iron-dependent lipid peroxidation, is closely associated with the occurrence and development of various diseases. Microcystin-LR (MC-LR) can exacerbate sepsis by causing multi-organ damage via the ferroptosis pathway. Currently, the relationship between MC-LR, ferroptosis, and sepsis remains unclear. Understanding its pathogenesis and identifying potential therapeutic targets may reduce the mortality of sepsis patients and lead to clinical improvement. This article reviews the relationship among MC-LR, ferroptosis, and sepsis, focusing on the mechanism by which MC-LR exposure induces sepsis from the ferroptosis perspective, providing a theoretical basis for the prevention and treatment of MC-LR-exposure-induced sepsis in the population.

摘要

脓毒症是一种由感染引发的全身性炎症反应综合征,其特点是起病急、进展快、死亡率高。铁死亡是一种由铁依赖性脂质过氧化诱导的程序性细胞死亡形式,与多种疾病的发生和发展密切相关。微囊藻毒素-LR(MC-LR)可通过铁死亡途径导致多器官损伤,从而加重脓毒症。目前,MC-LR、铁死亡与脓毒症之间的关系尚不清楚。了解其发病机制并确定潜在的治疗靶点可能会降低脓毒症患者的死亡率并改善临床状况。本文综述了MC-LR、铁死亡与脓毒症之间的关系,重点从铁死亡角度探讨MC-LR暴露诱导脓毒症的机制,为人群中MC-LR暴露诱导的脓毒症的预防和治疗提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/d6ab88cfd2b1/biomolecules-15-00947-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/e9f9a6afed0c/biomolecules-15-00947-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/2a82e98fa9fd/biomolecules-15-00947-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/3b2e79b0efc1/biomolecules-15-00947-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/f117324f984c/biomolecules-15-00947-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/d6ab88cfd2b1/biomolecules-15-00947-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/e9f9a6afed0c/biomolecules-15-00947-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/2a82e98fa9fd/biomolecules-15-00947-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/3b2e79b0efc1/biomolecules-15-00947-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/f117324f984c/biomolecules-15-00947-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ba/12292872/d6ab88cfd2b1/biomolecules-15-00947-g005.jpg

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本文引用的文献

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Int J Biol Sci. 2025 Feb 24;21(5):2179-2200. doi: 10.7150/ijbs.105446. eCollection 2025.
2
Shielding the Gut: Ghrelin and Ferrostatin-1's Protective Role Against Sepsis-Induced Intestinal Ferroptosis.保护肠道:胃饥饿素和铁死亡抑制因子-1对脓毒症诱导的肠道铁死亡的保护作用
Biomedicines. 2024 Dec 31;13(1):77. doi: 10.3390/biomedicines13010077.
3
Microcystin-LR induces lung injury in mice through the NF-κB/NLRP3 pathway.微囊藻毒素-LR通过NF-κB/NLRP3途径诱导小鼠肺损伤。
J Toxicol Environ Health A. 2025 May 19;88(10):385-394. doi: 10.1080/15287394.2024.2443525. Epub 2025 Jan 8.
4
Mitochondrial DNA-activated cGAS-STING pathway in cancer: Mechanisms and therapeutic implications.癌症中线粒体DNA激活的cGAS-STING通路:机制与治疗意义
Biochim Biophys Acta Rev Cancer. 2025 Feb;1880(1):189249. doi: 10.1016/j.bbcan.2024.189249. Epub 2024 Dec 17.
5
COX-2 optimizes cardiac mitochondrial biogenesis and exerts a cardioprotective effect during sepsis.COX-2 优化心肌线粒体生物发生并在脓毒症期间发挥心脏保护作用。
Cytokine. 2024 Oct;182:156733. doi: 10.1016/j.cyto.2024.156733. Epub 2024 Aug 10.
6
The regulation and function of Nrf2 signaling in ferroptosis-activated cancer therapy.Nrf2 信号在铁死亡激活的癌症治疗中的调控和功能。
Acta Pharmacol Sin. 2024 Nov;45(11):2229-2240. doi: 10.1038/s41401-024-01336-2. Epub 2024 Jul 17.
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Amentoflavone attenuates homocysteine-induced neuronal ferroptosis-mediated inflammatory response: Involvement of the SLC7A11/GPX4 axis activation.阿魏酸二甲酯减轻同型半胱氨酸诱导的神经元铁死亡介导的炎症反应:涉及 SLC7A11/GPX4 轴的激活。
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