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Cellular and Molecular Mechanisms in Gynecological Disorders—Second Edition
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Cellular and Molecular Mechanisms in Gynecological Disorders—Second Edition

A Special Issue of Cells (ISSN 2073-4409) belonging to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 March 2027 | Viewed by 7176

Editor

Dr. Qiwei Yang

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA
Interests: reproductive medicine; gynecology; cancer biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following the successful completion of the first edition of our Special Issue, titled “Cellular and Molecular Mechanisms in Gynecological Disorders”, we are pleased to announce the launch of its second edition. The strong interest and valuable contributions from researchers worldwide underscored the critical need to continue exploring the complex pathogenesis of gynecological disorders at the cellular and molecular levels.

Gynecological disorders encompass a broad spectrum of conditions affecting the female reproductive system, including the uterus, ovaries, fallopian tubes, cervix, and vagina. These disorders carry a significant burden on women's health and quality of life and contribute substantially to public health and healthcare costs globally. Despite ongoing research, the underlying causes and mechanisms remain poorly understood in many cases.

This second edition continues to focus on elucidating the cellular and molecular basis of gynecological diseases. We aim to highlight recent advances and encourage the submission of high-quality research and comprehensive reviews addressing key biological pathways, molecular targets, genomics, epigenomics, cell-type specificity, and systems-level analysis in these conditions.

We welcome submissions related to a wide range of gynecological disorders, including, but not limited to, the following: uterine diseases (adenomyosis, endometriosis, endometrial cancer, leiomyosarcoma, and uterine fibroids), ovary-related diseases (ovarian cancer, ovarian torsion, primary ovarian insufficiency, and polycystic ovary syndrome), and other conditions (infertility, breast cancer, and cervical and vaginal diseases).

Both basic and translational research studies are encouraged, with an emphasis on those offering insights into novel therapeutic targets or diagnostic biomarkers.

We look forward to your contributions and to advancing our understanding of women’s reproductive health through this collaborative effort.

Dr. Qiwei Yang
Guest Editor

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 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • uterus
  • ovary
  • fallopian tubes
  • cervix
  • vagina
  • endometriosis
  • polycystic ovary syndrome
  • primary ovarian insufficiency
  • ovarian cysts
  • adenomyosis
  • endometriosis
  • leiomyoma (uterine fibroids)
  • endometrial cancer
  • leiomyosarcoma
  • female infertility
  • breast cancer
  • cell atlas
  • biomarkers
  • stem cells
  • pathways
  • transcriptome
  • proteomics
  • epigenome

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Published Papers (3 papers)

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Research

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15 pages, 5582 KB  
Article
Serum Extracellular Vesicle Protein Signatures Associated with Early-Stage High-Grade Serous Ovarian Carcinoma
by Michelle Lightfoot, Kalpana Deepa Priya Dorayappan, Vignesh Vudatha, Lakshmi Narasimhan. Chakrapani, Priyam Das, Lianbo Yu, Colin Hisey, Takahiko Sakaue, Thangavel Muthusamy, Parthiban Panneerselvam, Floor Backes, Casey Cosgrove, Derek Hansford, David E. Cohn, David M. O’Malley, Rajan Gogna and Karuppaiyah Selvendiran
Cells 2026, 15(8), 706; https://doi.org/10.3390/cells15080706 - 16 Apr 2026
Cited by 1 | Viewed by 1099
Abstract
Background: High-grade serous ovarian carcinoma (HGSOC) is the most common and lethal subtype of epithelial ovarian cancer and is frequently diagnosed at advanced stages. Because currently available blood-based biomarkers have limited performance in early-stage disease, there is a need to identify circulating biomarker [...] Read more.
Background: High-grade serous ovarian carcinoma (HGSOC) is the most common and lethal subtype of epithelial ovarian cancer and is frequently diagnosed at advanced stages. Because currently available blood-based biomarkers have limited performance in early-stage disease, there is a need to identify circulating biomarker candidates associated with early-stage HGSOC. In this retrospective multi-institutional case–control study, we evaluated whether serum extracellular vesicle (EV)-associated protein signatures distinguish early-stage HGSOC from healthy controls. Methods: Serum samples (n = 252) were obtained retrospectively from multiple institutions and included healthy controls and patients with early- and advanced-stage HGSOC. EV-associated proteins were profiled using liquid chromatography–tandem mass spectrometry (LC–MS/MS) and proximity extension assay (PEA) to identify candidate proteins enriched in early-stage HGSOC. Selected candidates were evaluated by enzyme-linked immunosorbent assay (ELISA), and tissue-level expression was examined in early-stage HGSOC specimens. A multimarker combination model was generated using a smoothed empirical estimate of hyper-volume under the manifold (SHUM) approach and internally assessed by leave-one-out cross-validation. Results: Ten EV-associated serum proteins were prioritized on the basis of differential expression and fold change and were confirmed to be expressed in early-stage HGSOC tissues. In ELISA-based analyses, the combined 10-protein EV panel distinguished early-stage HGSOC from healthy controls with an area under the curve (AUC) of 0.99 in the study dataset, whereas MUC16 (CA-125) showed substantially lower performance in this comparison. The SHUM-based model yielded a true-positive rate of 0.971, a false-positive rate of 0.057, and a Matthews correlation coefficient of 0.915 in the analyzed cohort. Several candidate proteins were differentially enriched in EV fractions but not in matched whole serum. Conclusions: Serum EV-associated proteins are altered in early-stage HGSOC and define a multi-protein signature associated with this disease state in a retrospective case–control setting. These findings support further evaluation of EV-based biomarker candidates in clinically representative and prospectively collected cohorts that include benign gynecologic conditions, symptomatic patients, and pre-diagnostic samples. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders—Second Edition)
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Review

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50 pages, 853 KB  
Review
Endometrial Vitamin D Signaling and Immune Escape in Recurrent Pregnancy Loss
by Charalampos Voros, Fotios Chatzinikolaou, Georgios Papadimas, Ioannis Papapanagiotou, Nektaria Zagorianakou, Ali Can Gunes, Aristotelis-Marios Koulakmanidis, Athanasios Karpouzos, Kyriakos Bananis, Charalampos Tsimpoukelis, Maria Anastasia Daskalaki, Christina-Maria Trakatelli, Stylianos Makrydimas, Nikolaos Thomakos, Panagiotis Antsaklis, Dimitrios Loutradis and George Daskalakis
Cells 2026, 15(15), 1405; https://doi.org/10.3390/cells15151405 - 3 Aug 2026
Viewed by 492
Abstract
Recurrent pregnancy loss (RPL) continues to be a significant challenge in reproductive medicine, particularly in women for whom standard examinations do not reveal a conclusive underlying reason. There is growing evidence that several instances may result from nuanced alterations in the endometrial milieu, [...] Read more.
Recurrent pregnancy loss (RPL) continues to be a significant challenge in reproductive medicine, particularly in women for whom standard examinations do not reveal a conclusive underlying reason. There is growing evidence that several instances may result from nuanced alterations in the endometrial milieu, particularly with decidualization and maternal–fetal immune tolerance. In recent years, vitamin D has gained recognition for its significance in early pregnancy, serving not only as a regulator of calcium metabolism but also as an active contributor to endometrial and immunological functions. The human endometrium exhibits the vitamin D receptor (VDR) and the enzyme CYP27B1, facilitating the local activation and signaling of vitamin D inside the uterine milieu. Experimental investigations have shown that vitamin D influences many processes critical for effective implantation and placentation, including stromal cell differentiation, cytokine equilibrium, trophoblast invasion, oxidative stress responses, and immune cell communication. Aberrant vitamin D signaling has been associated with heightened inflammatory activity, impaired decidual transformation, altered uterine natural killer cell functionality, and alteration of the Treg/Th17 equilibrium, all of which have been implicated in recurrent pregnancy loss. Concurrently, there is an increasing emphasis on the association between vitamin D and mitochondrial function as well as oxidative stress in decidual and endometrial cells. Interruption of these pathways may influence implantation and early embryonic development by impacting cellular metabolism and immunological control at the maternal–fetal interface. The clinical interest in vitamin D supplementation for women experiencing repeated reproductive failure is increasing; nevertheless, the existing results are conflicting, mostly due to the predominance of research focusing on circulating vitamin D levels rather than localized tissue-specific processes. Our review encapsulates new findings about the function of vitamin D in endometrial biology and reproductive immune regulation, emphasizing its involvement in decidualization, inflammatory signaling, oxidative stress, and maternal–fetal immunological tolerance in recurrent pregnancy loss. The potential ramifications for assisted reproduction and forthcoming tailored therapy techniques are also examined. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders—Second Edition)
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22 pages, 1081 KB  
Review
Pseudouridine Synthase 7 in Cancer: Functions, Mechanisms, and Therapeutic Potential
by Qiwei Yang, Thomas G. Boyer and Ayman Al-Hendy
Cells 2025, 14(17), 1380; https://doi.org/10.3390/cells14171380 - 4 Sep 2025
Cited by 12 | Viewed by 4593
Abstract
Pseudouridylation, the most abundant RNA modification, plays a critical role in modulating RNA structure, stability, and function. Among the family of pseudouridine synthases, Pseudouridine Synthase 7 (PUS7) has recently gained attention for its emerging roles in human health and disease. Originally characterized for [...] Read more.
Pseudouridylation, the most abundant RNA modification, plays a critical role in modulating RNA structure, stability, and function. Among the family of pseudouridine synthases, Pseudouridine Synthase 7 (PUS7) has recently gained attention for its emerging roles in human health and disease. Originally characterized for its function in modifying tRNA and small non-coding RNAs, PUS7 is now recognized as a dynamic regulator of mRNA pseudouridylation, influencing gene expression at the post-transcriptional level. Aberrant expressions or activity of PUS7 have been linked to a variety of pathological conditions, including cancers such as colon cancer, glioblastoma, pancreatic cancer, and neuroblastoma, as well as potential roles in neurodevelopmental disorders and immune regulation. Through mechanisms involving translational reprogramming, stress adaptation, and epitranscriptomic remodeling, PUS7 contributes to disease progression and cellular plasticity. This review summarizes the current understanding of PUS7 biology, its functional relevance in the contexts of cancer progression, and the growing interest in targeting RNA-modifying enzymes for therapeutic intervention. Uncovering the full spectrum of PUS7-mediated pseudouridylation and its downstream effects holds promise for advancing our understanding of RNA-based regulation in human diseases, including gynecological disorders. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders—Second Edition)
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