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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 May 2026 | Viewed by 7490

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

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Keywords

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

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Published Papers (4 papers)

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Research

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16 pages, 2620 KB  
Article
Copper-Targeted Therapy in Experimental Endometriosis: Effects of Ammonium Tetrathiomolybdate on Markers of the Interconnected Processes of Inflammation, Innervation, and Fibrogenesis
by María Belén Delsouc, Rocío Ayelem Conforti, Ana Sofia Zabala, Verónica Palmira Filippa, Leonardo Mariño-Repizo, Sandra Silvina Vallcaneras and Marilina Casais
Int. J. Mol. Sci. 2026, 27(2), 1099; https://doi.org/10.3390/ijms27021099 - 22 Jan 2026
Viewed by 535
Abstract
Endometriosis (EDT) is a chronic, estrogen-dependent disease characterized by inflammation, fibrosis, pelvic pain, and infertility. Current therapies show limited long-term efficacy and adverse effects, underscoring the need for novel therapeutic approaches. Elevated copper (Cu) levels have been reported in both patients and animal [...] Read more.
Endometriosis (EDT) is a chronic, estrogen-dependent disease characterized by inflammation, fibrosis, pelvic pain, and infertility. Current therapies show limited long-term efficacy and adverse effects, underscoring the need for novel therapeutic approaches. Elevated copper (Cu) levels have been reported in both patients and animal models of EDT, making Cu chelation a promising strategy. This work aimed to evaluate the impact of ammonium tetrathiomolybdate (TM) on the expression of markers related to the interconnected processes of inflammation, innervation, and fibrogenesis in mice with induced EDT. Twenty-four female C57BL/6 mice were assigned to Sham, EDT, or EDT+TM groups. Treatment with TM began on postoperative day 15, with samples collected one month after EDT induction. Peritoneal fluid cytokines (TNF-α, IL-1β, IL-6, TGF-β1) were quantified by ELISA. Endometriotic-like lesions were examined for mRNA expression of cytokines, neurotrophins (Ngf, Bdnf, Ngfr), neural markers (Uchl1, Gap43), neuropeptides and nociceptive markers (Tac1/Tacr1, Calca/Calcrl/Ramp1, Trpv1), and fibrogenic markers (Vim, Acta2, Col1a1, Fmod) by RT-qPCR. Neurotrophin protein levels were measured by ELISA, and collagen content was assessed through Masson’s staining. TM significantly modulated inflammatory, neural, nociceptive, and fibrogenic markers, reducing most of them along with collagen content. These findings suggest that TM could impact key pathological mechanisms involved in EDT. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis)
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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 1252
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 2072
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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Review

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39 pages, 1187 KB  
Review
Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy
by Daniel Simancas-Racines, Emilia Jiménez-Flores, Martha Montalvan, Raquel Horowitz, Valeria Araujo and Claudia Reytor-González
Int. J. Mol. Sci. 2026, 27(2), 908; https://doi.org/10.3390/ijms27020908 - 16 Jan 2026
Cited by 4 | Viewed by 2905
Abstract
Endometriosis is traditionally conceptualized as a pelvic lesion–centered disease; however, mounting evidence indicates it is a chronic, systemic, and multifactorial inflammatory disorder. This review examines the molecular dialog between ectopic endometrial tissue, the immune system, and peripheral organs, highlighting mechanisms that underlie disease [...] Read more.
Endometriosis is traditionally conceptualized as a pelvic lesion–centered disease; however, mounting evidence indicates it is a chronic, systemic, and multifactorial inflammatory disorder. This review examines the molecular dialog between ectopic endometrial tissue, the immune system, and peripheral organs, highlighting mechanisms that underlie disease chronicity, symptom variability, and therapeutic resistance. Ectopic endometrium exhibits distinct transcriptomic and epigenetic signatures, disrupted hormonal signaling, and a pro-inflammatory microenvironment characterized by inflammatory mediators, prostaglandins, and matrix metalloproteinases. Immune-endometrial crosstalk fosters immune evasion through altered cytokine profiles, extracellular vesicles, immune checkpoint molecules, and immunomodulatory microRNAs, enabling lesion persistence. Beyond the pelvis, systemic low-grade inflammation, circulating cytokines, and microRNAs reflect a molecular spillover that contributes to chronic pain, fatigue, hypothalamic–pituitary–adrenal axis dysregulation, and emerging gut–endometrium interactions. Furthermore, circulating biomarkers—including microRNAs, lncRNAs, extracellular vesicles, and proteomic signatures—offer potential for early diagnosis, patient stratification, and monitoring of therapeutic responses. Conventional hormonal therapies demonstrate limited efficacy, whereas novel molecular targets and delivery systems, including angiogenesis inhibitors, immune modulators, epigenetic regulators, and nanotherapeutics, show promise for precision intervention. A systems medicine framework, integrating multi-omics analyses and network-based approaches, supports reconceptualizing endometriosis as a systemic inflammatory condition with gynecologic manifestations. This perspective emphasizes the need for interdisciplinary collaboration to advance diagnostics, therapeutics, and individualized patient care, ultimately moving beyond a lesion-centered paradigm toward a molecularly informed, holistic understanding of endometriosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Biomarkers, and Therapeutic Targets for Endometriosis)
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