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铁死亡作为通过脂质过氧化抑制肿瘤的新工具。

Ferroptosis as a new tool for tumor suppression through lipid peroxidation.

机构信息

Suzhou Ninth Hospital Affiliated to Soochow University, The Institutes of Biology and Medical Sciences, Suzhou Medical College, Soochow University, Suzhou, Jiangsu, China.

Institute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians & Surgeons, Columbia University, New York, NY, USA.

出版信息

Commun Biol. 2024 Nov 9;7(1):1475. doi: 10.1038/s42003-024-07180-8.

DOI:10.1038/s42003-024-07180-8
PMID:39521912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11550846/
Abstract

As a newly defined type of programmed cell death, ferroptosis is considered a potent weapon against tumors due to its distinct mechanism from other types of programmed cell death. Ferroptosis is triggered by the uncontrolled accumulation of hydroperoxyl polyunsaturated fatty acid-containing phospholipids, also called lipid peroxidation. The lipid peroxidation, generated through enzymatic and non-enzymatic mechanisms, drives changes in cell morphology and the destruction of membrane integrity. Here, we dissect the mechanisms of ferroptosis induced enzymatically or non-enzymatically, summarize the major metabolism pathways in modulating lipid peroxidation, and provide insights into the relationship between ferroptosis and tumor suppression. In this review, we discuss the recent advances of ferroptosis in tumor microenvironments and the prospect of potential therapeutic application.

摘要

铁死亡作为一种新定义的细胞程序性死亡方式,由于其与其他类型细胞程序性死亡的机制不同,被认为是对抗肿瘤的有力武器。铁死亡是由过氧氢聚不饱和脂肪酸含磷脂的不受控制的积累引起的,也称为脂质过氧化。通过酶和非酶机制产生的脂质过氧化作用,导致细胞形态的变化和膜完整性的破坏。在这里,我们剖析了酶促或非酶促诱导铁死亡的机制,总结了调节脂质过氧化的主要代谢途径,并深入探讨了铁死亡与肿瘤抑制之间的关系。在这篇综述中,我们讨论了铁死亡在肿瘤微环境中的最新进展及其潜在治疗应用的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/5b05054547ee/42003_2024_7180_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/35f5e04063a0/42003_2024_7180_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/3511517b2085/42003_2024_7180_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/c66b08a2dcb6/42003_2024_7180_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/8915043d2e3c/42003_2024_7180_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/5b05054547ee/42003_2024_7180_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/35f5e04063a0/42003_2024_7180_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/3511517b2085/42003_2024_7180_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/c66b08a2dcb6/42003_2024_7180_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/8915043d2e3c/42003_2024_7180_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9bb/11550846/5b05054547ee/42003_2024_7180_Fig5_HTML.jpg

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Phospholipid peroxidation in macrophage confers tumor resistance by suppressing phagocytic capability towards ferroptotic cells.
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