Dysregulated autophagy in endometriosis: molecular mechanisms, controversies, and clinical implications

Clara Tellez-Quijorna, Ainhoa Juan-Lopez, Núria Eritja, Nuria Eritja, David Llobet-Navas, David Llobet‐Navàs, Laura Devis, Laura Devis-Jauregui
Reproductive biology and endocrinology : RB&E · 2025 · vol. 24(1) , pp. 8 · doi:10.1186/s12958-025-01494-w · PMID:41388415 · PMC12821204 · W4417289728
review OA: gold CC0 ⤵ 1 in-corpus citation
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review highlights research on the dysregulated autophagy process in endometriosis, exploring its molecular mechanisms, controversies in findings, and potential as a therapeutic target.

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Abstract

Endometriosis is one of the most common gynecological diseases in women and is still one of the most understudied diseases, affecting the daily lives of patients. Although the exact cause of this condition remains unclear, autophagy has been proposed as a potential biological process involved in the disease. Autophagy is a highly conserved catabolic process crucial for the degradation of lysosomes and several cellular components. In recent years, various studies have shown that this biological process could be crucial in endometriosis, with some evidence demonstrating its upregulation and others its downregulation in different study models. Due to this controversy and the potential implications of autophagy as a therapeutic target, this current review highlights significant findings on the involvement of autophagy in endometriosis and explores its potential as a therapeutic target.

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Condition tags

endometriosis

MeSH descriptors

Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (1)

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