Evidence map›Paper›PMID 41388415›Full record

ReviewReproductive biology and endocrinology : RB&E2025

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

Clara Tellez-Quijorna, Ainhoa Juan-Lopez, Nuria Eritja, David Llobet-Navas, Laura Devis-Jauregui

Abstract readReview
In one paragraph

Review in Reproductive biology and endocrinology : RB&E, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Clara Tellez-QuijornaIntegrative molecular biology in hematopoiesis and leukemia, Equipe Labellisée Ligue Contre le Cancer, CRCM, Inserm UMR1068, CNRS UMR7258, Institut Paoli-Calmettes, Aix Marseille Univ, Marseille, France.
Ainhoa Juan-LopezDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain.
Nuria EritjaDepartment of Medicine and Surgery, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), Lleida, 25198, Spain.
David Llobet-NavasCentro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, (ISCIII), Madrid, 28029, Spain.
Laura Devis-JaureguiDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. ldevisjauregui@ub.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AutophagyEndometriosisAnimalsFemaleHumansLysosomesAutophagyDysregulated autophagyEctopic endometriumEndometriosisEutopic endometriumTherapeutic targeting

Identifiers

PMID41388415
PMCPMC12821204

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.