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Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis
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Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 2236

Special Issue Editors

Dr. Katharina Proestling

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria
Interests: primary endometrial stroma cells; endometriosis; epigenetics, signaling, endocrinology and metabolism
Dr. Iveta Yotova

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria
Interests: endometriosis; lncRNAs; imprinting; epigenetics; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endometriosis is a chronic gynecological disease marked by ectopic endometrial-like tissue growth, often causing pain, infertility, and compromised quality of life. The disease pathogenesis involves complex molecular mechanisms, including epigenetic, hormonal, and immunological dysregulation, oxidative stress, chronic inflammation, and fibrogenesis. As the exact mechanisms remain elusive, this Special Issue aims to advance our understanding that eventually could improve the development of novel therapeutic approaches.

While recent advancements emphasize non-invasive diagnostic imaging techniques, particularly magnetic resonance imaging (MRI) and ultrasound, they cannot replace surgery in diagnosing all subtypes of endometriosis. Potential studies that hold promise for non-invasive biomarkers for diagnosing endometriosis and/or progression, such as epigenetic regulators, gene profiles, or specific proteins, will be published in this Special Issue and could eventually complement imaging for a comprehensive, non-invasive diagnostic approach.

Dr. Katharina Proestling
Dr. Iveta Yotova
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • endometriosis
  • biomarkers
  • inflammation
  • fibrosis
  • oxidative stress
  • epigenetics

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Published Papers (2 papers)

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Research

16 pages, 2697 KB  
Article
Growth Arrest-Specific Protein 6 Is Elevated in Endometriosis but Shows Poor Diagnostic Performance
by Maja Novak Pušić, Robert Marijan, Teja Klančič, Tamara Knific, Helena Ban Frangež and Tea Lanišnik Rižner
Int. J. Mol. Sci. 2025, 26(17), 8348; https://doi.org/10.3390/ijms26178348 - 28 Aug 2025
Viewed by 573
Abstract
Growth arrest-specific protein 6 (GAS6) has an important role in regulating the immune system. Recent studies have revealed its association with the pathophysiology of endometriosis and identified GAS6 as one of the hub genes and a biomarker candidate. Endometriosis is a common chronic [...] Read more.
Growth arrest-specific protein 6 (GAS6) has an important role in regulating the immune system. Recent studies have revealed its association with the pathophysiology of endometriosis and identified GAS6 as one of the hub genes and a biomarker candidate. Endometriosis is a common chronic inflammatory gynaecological disease of women of childbearing age. Due to surgical diagnosis, non-invasive biomarkers are urgently needed. We investigated GAS6 as a candidate biomarker for the diagnosis of endometriosis. Our case–control study included 284 patients and showed that plasma levels of GAS6 are significantly higher in patients with endometriosis compared to control patients. We calculated logistic regression models using GAS6, CA-125, and GAS6 together with CA-125, and added a series of clinical and lifestyle data collected before surgical diagnosis. A CA-125 model and a model including GAS6 and CA-125 showed the highest AUC values of 0.745 ± 0.04, while the model including CA-125, data on sport/recreation before surgery, and dysmenorrhea score reached an AUC of 0.767 ± 0.04. Our results indicate that GAS6 is increased in patients with endometriosis, but it cannot serve as a biomarker candidate. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis)
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17 pages, 3752 KB  
Article
Disease Severity- and Hormonal Status-Dependent Alterations of EGF and MIF in the Serum of Endometriosis Patients
by Norbert Tóth, Réka Brubel, Attila Bokor, Ágnes Kemény, Nelli Farkas, Tibor Pál, Zsuzsanna Helyes and Krisztina Pohóczky
Int. J. Mol. Sci. 2025, 26(14), 6695; https://doi.org/10.3390/ijms26146695 - 12 Jul 2025
Viewed by 1153
Abstract
Endometriosis is the extrauterine engraftment of endometrium-like tissue, causing chronic pain. Complex sensory–vascular–immune interactions, including growth factors, cytokines, and neuropeptides, are implicated in its pathophysiology, but the mechanisms remain unknown. Here, epidermal growth factor (EGF), vascular endothelial growth factor, interleukins (IL-1β, IL-6, IL-8), [...] Read more.
Endometriosis is the extrauterine engraftment of endometrium-like tissue, causing chronic pain. Complex sensory–vascular–immune interactions, including growth factors, cytokines, and neuropeptides, are implicated in its pathophysiology, but the mechanisms remain unknown. Here, epidermal growth factor (EGF), vascular endothelial growth factor, interleukins (IL-1β, IL-6, IL-8), macrophage migration inhibitory factor (MIF), calcitonin gene-related peptide, and somatostatin were measured in the serum of endometriosis patients with different disease severities, menstruation cycle- and pharmacotherapy-related hormonal status compared with controls. Mediator levels in deep-infiltrating rectosigmoid nodules were also compared with those in non-endometriotic colon tissues. Pain was assessed by the visual analogue scale. Serum EGF was significantly lower in mild endometriosis and in the secretory phase. MIF and IL-6 were higher in stage I–IV endometriosis, with MIF also higher in the secretory phase and in patients not receiving oral contraceptives. Somatostatin was lower in mild endometriosis than that in healthy individuals and the severe endometriosis group. No tissue-level differences were found. A strong positive correlation between serum EGF and somatostatin levels and dysmenorrhea and dysuria was detected in mild cases. It is concluded that certain serum alterations may be related to severity- and hormone status-dependent endometriosis mechanisms, but their diagnostic/prognostic value seems to be limited due to variability and lack of specificity. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis)
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