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铁死亡:子宫内膜异位症发病机制与治疗中的新途径。

Ferroptosis: a novel pathway in the pathogenesis and treatment of endometriosis.

作者信息

Cheng Xunshu, Memon Muhammad Azhar, Ali Waseem, Ma Yonggang

机构信息

Sichuan University of Arts and Science, 635000, Dashon, People's Republic of China.

College of Veterinary Medicine, Yangzhsou University, Yangzhou, 225009, Jiangsu, People's Republic of China.

出版信息

J Mol Histol. 2025 Aug 22;56(5):272. doi: 10.1007/s10735-025-10499-z.

DOI:10.1007/s10735-025-10499-z
PMID:40844669
Abstract

As a common chronic disease, endometriosis (EMs) affects nearly 10% of women of childbearing age, may cause other complications such as infertility, and has a tendency to develop malignant tumors. Ferroptosis is a newly discovered apoptotic process characterized by intracellular free iron excess, which mediates Fenton reaction and eventually leads to lipid peroxidation in the cell membrane leading to cell death. The abnormal changes of intracellular iron concentration may lead to the accumulation of reactive oxygen species (ROS) and the imbalance of redox homeostasis, thus leading to the occurrence of iron death. At present, the pathogenesis and effect of iron death on EMs are not completely clear, and the study of its physiological and pathological mechanism is very important for its diagnosis and treatment. This article reviews the research progress of the occurrence and development of EMs in order to provide new ideas for the pathogenesis, diagnosis and treatment of EMs.

摘要

作为一种常见的慢性病,子宫内膜异位症(EMs)影响着近10%的育龄女性,可能引发不孕等其他并发症,且有发展为恶性肿瘤的倾向。铁死亡是一种新发现的凋亡过程,其特征是细胞内游离铁过量,介导芬顿反应,最终导致细胞膜脂质过氧化,从而导致细胞死亡。细胞内铁浓度的异常变化可能导致活性氧(ROS)积累和氧化还原稳态失衡,进而引发铁死亡。目前,铁死亡在EMs中的发病机制和作用尚不完全清楚,对其生理和病理机制的研究对其诊断和治疗非常重要。本文综述了EMs发生发展的研究进展,以期为EMs的发病机制、诊断和治疗提供新思路。

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本文引用的文献

1
Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics.铁死亡:聚氯乙烯微塑料诱导早产鸭卵巢的初步证据。
Sci Total Environ. 2024 Jul 10;933:173032. doi: 10.1016/j.scitotenv.2024.173032. Epub 2024 May 9.
2
Liproxstatin-1 attenuates acute hypertriglyceridemic pancreatitis through inhibiting ferroptosis in rats.脂氧素A1通过抑制大鼠铁死亡减轻急性高甘油三酯血症性胰腺炎。
Sci Rep. 2024 Apr 25;14(1):9548. doi: 10.1038/s41598-024-60159-7.
3
PRMT4 interacts with NCOA4 to inhibit ferritinophagy in cisplatin-induced acute kidney injury.
PRMT4 与 NCOA4 相互作用,抑制顺铂诱导的急性肾损伤中的铁蛋白自噬。
FASEB J. 2024 Apr 15;38(7):e23584. doi: 10.1096/fj.202302596R.
4
Cryptochrome 1 regulates ovarian granulosa cell senescence through NCOA4-mediated ferritinophagy.隐花色素1通过NCOA4介导的铁蛋白自噬调节卵巢颗粒细胞衰老。
Free Radic Biol Med. 2024 May 1;217:1-14. doi: 10.1016/j.freeradbiomed.2024.03.015. Epub 2024 Mar 22.
5
Ferroptosis and oxidative stress in endometriosis: A systematic review of the literature.内异症中的铁死亡和氧化应激:文献系统综述。
Medicine (Baltimore). 2024 Mar 15;103(11):e37421. doi: 10.1097/MD.0000000000037421.
6
Non-apoptotic cell death programs in cervical cancer with an emphasis on ferroptosis.宫颈癌中的非凋亡性细胞死亡程序,重点是铁死亡。
Crit Rev Oncol Hematol. 2024 Feb;194:104249. doi: 10.1016/j.critrevonc.2023.104249. Epub 2023 Dec 23.
7
Omics-based novel strategies in the diagnosis of endometriosis.基于组学的子宫内膜异位症诊断新策略。
Crit Rev Clin Lab Sci. 2024 May;61(3):205-225. doi: 10.1080/10408363.2023.2270736. Epub 2023 Oct 25.
8
Suberosin Alleviates Thiazolidinedione-Induced Cardiomyopathy in Diabetic Rats by Inhibiting Ferroptosis via Modulation of ACSL4-LPCAT3 and PI3K-AKT Signaling Pathways.亚油酸酰胺通过调节 ACSL4-LPCAT3 和 PI3K-AKT 信号通路抑制铁死亡缓解噻唑烷二酮诱导的糖尿病大鼠心肌病。
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