Role of autophagy and ferroptosis in the development of endometriotic cysts (Review).

IF 5.7 3区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
International journal of molecular medicine Pub Date : 2024-09-01 Epub Date: 2024-07-12 DOI:10.3892/ijmm.2024.5402
Hiroshi Kobayashi, Shogo Imanaka, Chiharu Yoshimoto, Sho Matsubara, Hiroshi Shigetomi
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引用次数: 0

Abstract

It is considered that the etiology of endometriosis is retrograde menstruation of endometrial tissue. Although shed endometrial cells are constantly exposed to a challenging environment with iron overload, oxidative stress and hypoxia, a few cells are able to survive and continue to proliferate and invade. Ferroptosis, an iron‑dependent form of non‑apoptotic cell death, is known to play a major role in the development and course of endometriosis. However, few papers have concentrated on the dynamic interaction between autophagy and ferroptosis throughout the progression of diseases. The present review summarized the current understanding of the mechanisms underlying autophagy and ferroptosis in endometriosis and discuss their role in disease development and progression. For the present narrative review electronic databases including PubMed and Google Scholar were searched for literature published up to the October 31, 2023. Autophagy and ferroptosis may be activated at early stages in endometriosis development. On the other hand, excessive activation of intrinsic pathways (e.g., estrogen and mechanistic target of rapamycin) may promote disease progression through autophagy inhibition. Furthermore, suppression of ferroptosis may cause further progression of endometriotic lesions. In conclusion, the autophagy and ferroptosis pathways may play a dual role in disease initiation and progression. The present review discussed the temporal transition of non‑apoptotic cell death regulation during disease progression from retrograde endometrium to early lesions to established lesions.

自噬和铁变态在子宫内膜异位囊肿发展中的作用(综述)。
子宫内膜异位症的病因被认为是子宫内膜组织的逆行月经。虽然脱落的子宫内膜细胞不断暴露在铁超载、氧化应激和缺氧的挑战性环境中,但仍有少数细胞能够存活下来,并继续增殖和入侵。铁凋亡是一种铁依赖的非凋亡性细胞死亡形式,已知在子宫内膜异位症的发展和病程中起着重要作用。然而,很少有论文集中研究自噬和铁凋亡在疾病进展过程中的动态相互作用。本综述总结了目前对子宫内膜异位症中自噬和铁吞噬机制的理解,并讨论了它们在疾病发展和进程中的作用。本综述在电子数据库(包括PubMed和谷歌学术)中检索了截至2023年10月31日发表的文献。在子宫内膜异位症发展的早期阶段,自噬和铁变态反应可能会被激活。另一方面,内在途径(如雌激素和雷帕霉素机理靶点)的过度激活可能会通过抑制自噬促进疾病进展。此外,抑制铁变态反应可能会导致子宫内膜异位症病变进一步恶化。总之,自噬和铁蛋白沉积途径可能在疾病的发生和发展中扮演着双重角色。本综述讨论了从逆行性子宫内膜到早期病变再到成熟病变的疾病进展过程中,非凋亡性细胞死亡调控的时间过渡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
International journal of molecular medicine
International journal of molecular medicine 医学-医学:研究与实验
CiteScore
12.30
自引率
0.00%
发文量
124
审稿时长
3 months
期刊介绍: The main aim of Spandidos Publications is to facilitate scientific communication in a clear, concise and objective manner, while striving to provide prompt publication of original works of high quality. The journals largely concentrate on molecular and experimental medicine, oncology, clinical and experimental cancer treatment and biomedical research. All journals published by Spandidos Publications Ltd. maintain the highest standards of quality, and the members of their Editorial Boards are world-renowned scientists.
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