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Endometriosis: Current Trends and Research Developments
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Endometriosis: Current Trends and Research Developments

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 31 January 2027 | Viewed by 3830

Editors

Prof. Dr. Sylvia Mechsner

E-Mail Website
Guest Editor
Department of Gynecology Charité with Center of Oncological Surgery, Endometriosis Research Center Charité, Berlin, Germany
Interests: molecular mechanisms of endometriosis pathogenesis; pain generation and neuromodulation; self‑management; mental health; patient‑centered care
Special Issues, Collections and Topics in MDPI journals
Dr. Renata Voltolini Velho

E-Mail Website
Guest Editor
Department of Gynecology Charité with Center of Oncological Surgery, Endometriosis Research Center Charité, Berlin, Germany
Interests: molecular mechanisms of endometriosis pathogenesis; pain generation and neuromodulation; analgesic targets; diagnostic tests

Special Issue Information

Dear Colleagues,

Endometriosis is a chronic, often debilitating, condition with a complex and multifactorial pathophysiology. Despite its high prevalence, the underlying molecular mechanisms remain insufficiently understood, limiting effective diagnostics and treatment. This Special Issue will bring together cutting-edge research elucidating the pathomechanisms of endometriosis through integrative, interdisciplinary approaches to molecular science. We welcome studies exploring hormonal regulation, immune modulation, genetic and epigenetic alterations, environmental factors, cell signaling, and tissue remodeling relevant to endometriosis.

Given the scope of IJMS, purely clinical studies are not suitable for this Special Issue. However, submissions based on patient cohorts, clinical samples, or in vitro/in vivo models are encouraged, provided that they include robust biomolecular experimentation, such as transcriptomic, proteomic, or metabolomic analyses; molecular pathway interrogation; or functional genomics.

This Special Issue will promote innovative biomolecular insights to inform future diagnostics, therapeutic strategies, and personalized medicine approaches in endometriosis research.

Prof. Dr. Sylvia Mechsner
Dr. Renata Voltolini Velho
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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
  • molecular mechanisms
  • pathophysiology
  • hormonal regulation
  • immune response
  • epigenetics
  • inflammation
  • biomarkers
  • transcriptomics
  • therapeutic targets

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Published Papers (2 papers)

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Research

18 pages, 3732 KB  
Article
Functional Analysis of the Histidine N-Methyltransferase SETD3 in Endometriosis
by Melanie Poloczek, Carolin Lisa Michaela Ludwig, Hanna Surmann, Theresa Strauß, Michael Gabriel, Matti Poutanen, Julia Oto, Ludwig Kiesel, Sebastian D. Schäfer, Lars Hanker, Joachim M. Weitzel and Martin Götte
Int. J. Mol. Sci. 2026, 27(13), 6069; https://doi.org/10.3390/ijms27136069 - 7 Jul 2026
Viewed by 858
Abstract
Endometriosis is a disease associated with pain symptoms and reduced fertility, characterized by the presence of endometrial tissue outside the uterus. SETD3 is an actin-specific histidine N-methyltransferase that regulates actin stability and flexibility. Here, we investigate the effects of altered SETD3 expression on [...] Read more.
Endometriosis is a disease associated with pain symptoms and reduced fertility, characterized by the presence of endometrial tissue outside the uterus. SETD3 is an actin-specific histidine N-methyltransferase that regulates actin stability and flexibility. Here, we investigate the effects of altered SETD3 expression on cytoskeletal function and endometriotic cell motility. SETD3 expression in endometriotic lesions was analyzed using EndometDB, and in uteri of the superfertile Dummerstorf mouse line FL1 by RT-qPCR. The functional impact of siRNA-mediated SETD3 depletion on endometriotic 12Z cells and primary endometriotic stroma cells was studied in vitro. Cell motility, contractility, invasiveness, morphology and gene expression were analyzed by RT-qPCR, Western blotting, immunofluorescence, scratch wound, collagen contraction and Matrigel invasion assays. In patient tissue, SETD3 expression was slightly increased in deep endometriotic lesions, whereas SETD3 was downregulated 1.6-fold in the uteri of superfertile mice. SETD3 depletion delayed cell motility, reduced invasiveness of 12Z cells, and reduced the capability to contract collagen gels. Cytoskeletal gene expression was moderately changed. Our data suggest that the histidine N-methyltransferase SETD3 contributes to cytoskeletal remodeling that plays a key role in cell migration and invasion. A dysregulation of SETD3 could therefore be related to the pathogenesis of endometriosis, particularly in deep endometriosis. Full article
(This article belongs to the Special Issue Endometriosis: Current Trends and Research Developments)
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19 pages, 2206 KB  
Article
The Histamine-Associated Inflammatory Landscape of Endometriosis: Molecular Profiling of HDC, HRH1-HRH4, and Cytokines Across Lesion Subtypes
by Renata Voltolini Velho, Julia Hannah Freitag, Arie Maeve Brueckner, Laura Thalmeier, Jonathan Pohl and Sylvia Mechsner
Int. J. Mol. Sci. 2026, 27(1), 212; https://doi.org/10.3390/ijms27010212 - 24 Dec 2025
Cited by 3 | Viewed by 2275
Abstract
Pain in endometriosis involves not only nociceptive but also neuropathic and neurogenic components, reflecting its complex nature. Histamine, a biogenic amine, has emerged as a critical mediator connecting inflammation and nerve sensitization. This study aimed to characterize histamine receptor (HRH1–HRH4) expression, localization, and [...] Read more.
Pain in endometriosis involves not only nociceptive but also neuropathic and neurogenic components, reflecting its complex nature. Histamine, a biogenic amine, has emerged as a critical mediator connecting inflammation and nerve sensitization. This study aimed to characterize histamine receptor (HRH1–HRH4) expression, localization, and related inflammatory mediators in peritoneal, deep infiltrating, and ovarian endometriosis. Gene expression datasets were analyzed, and immunofluorescence staining of endometriotic lesions was performed using immune and neuronal markers. Histamine and its metabolite methylhistamine were quantified in serum, peritoneal fluid, and urine samples. HDC expression was significantly elevated in all endometriotic lesions compared with controls (all p < 0.01), paralleling increased IL-6, COX-2, NGF, and NGFR levels (p < 0.0001). In contrast, HRH1–HRH4 transcript levels showed no significant differences between groups. Immunofluorescence demonstrated robust HRH1–HRH4 protein expression in epithelial, immune, and nerve fibers, with subtype-specific colocalization patterns. Serum histamine concentrations were significantly higher in endometriosis patients than controls (0.484 vs. 0.153 ng/mg protein; p = 0.0014), whereas peritoneal histamine and urinary methylhistamine showed no group differences. Overall, these findings highlight histamine signaling as a potentially important component of endometriosis pathophysiology and point toward new directions for mechanistic studies and therapeutic exploration. Full article
(This article belongs to the Special Issue Endometriosis: Current Trends and Research Developments)
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