Cellular and Molecular Mechanisms of Endometriosis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 7251

Special Issue Editors


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Guest Editor
Department of Women's and Children's Health—SDB, University of Padova, Via Giustiniani 2, 35131 Padova, Italy
Interests: protein purification; protein tyr-phosphorylation and dephosphorylation; inflammatory and metabolic dìseases; oxidative stress; eryptosis
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Guest Editor
Department of Women's and Children's Health—SDB, University of Padova, Via Giustiniani 2, 35131 Padova, Italy
Interests: endometriosis; ovarian

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Guest Editor
Department of Medicine—Endocrinology Unit, Hospital University of Padua, 35131 Padova, Italy
Interests: hypertension; renin-angiotensin system; polycystic ovary syndrome (PCOS); metabolic syndrome; hyperaldosteronism; autoimmune disease; addison disease; adrenal insufficiency

Special Issue Information

Dear Colleagues,

The presence of endometrial-like tissue (that is, the tissue that lines the uterine cavity) outside of the uterus is the common definition for endometriosis, characterized by three recognized phenotypes: superficial peritoneal lesions (SUP), ovarian endometriomas (OMA) and deep infiltrating endometriosis (DIE).

Recent advances in the mechanisms, diagnosis and management of endometriosis set the concept of the endometriosis life context, as a 360-degree approach to understanding and treating this disease.

The focus of this Special Issue of Biomolecules will be on the most recent advances, theories and biomarkers, from inflammation-related immune system activation to genetic/epigenetic involvement to the associated comorbidities and potential new treatments.

Dr. Luciana Bordin
Dr. Alessandra Andrisani
Dr. Chiara Sabbadin
Guest Editors

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Keywords

  • endocrine dysfunction in endometriosis
  • glycosylphosphatidylinositols (GPIs) and GPI-anchored proteins
  • oxidative stress markers (glutathione, carbonic anhydrase, etc.)
  • endometriosis and deep endometriosis
  • endometriosis-related immune system

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Published Papers (4 papers)

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Research

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13 pages, 7099 KiB  
Article
Assessment of the Ferroptosis Regulators: Glutathione Peroxidase 4, Acyl-Coenzyme A Synthetase Long-Chain Family Member 4, and Transferrin Receptor 1 in Patient-Derived Endometriosis Tissue
by Lidia A. Mielke Cabello, Gabriela Meresman, Dogus Darici, Noelia Carnovale, Birthe Heitkötter, Miriam Schulte, Nancy A. Espinoza-Sánchez, Quang-Khoi Le, Ludwig Kiesel, Sebastian D. Schäfer and Martin Götte
Biomolecules 2024, 14(7), 876; https://doi.org/10.3390/biom14070876 - 21 Jul 2024
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Abstract
Ferroptosis, an iron-dependent form of non-apoptotic cell death, plays a pivotal role in various diseases and is gaining considerable attention in the realm of endometriosis. Considering the classical pathomechanism theories, we hypothesized that ferroptosis, potentially driven by increased iron content at ectopic sites, [...] Read more.
Ferroptosis, an iron-dependent form of non-apoptotic cell death, plays a pivotal role in various diseases and is gaining considerable attention in the realm of endometriosis. Considering the classical pathomechanism theories, we hypothesized that ferroptosis, potentially driven by increased iron content at ectopic sites, may contribute to the progression of endometriosis. This retrospective case–control study provides a comprehensive immunohistochemical assessment of the expression and tissue distribution of established ferroptosis markers: GPX4, ACSL4, and TfR1 in endometriosis patients. The case group consisted of 38 women with laparoscopically and histologically confirmed endometriosis and the control group consisted of 18 women with other gynecological conditions. Our study revealed a significant downregulation of GPX4 in stromal cells of endometriosis patients (M = 59.7% ± 42.4 versus 90.0% ± 17.5 in the control group, t (54) = −2.90, p = 0.005). This finding aligned with slightly, but not significantly, higher iron levels detected in the blood of endometriosis patients, using hemoglobin as an indirect predictor (Hb 12.8 (12.2–13.5) g/dL versus 12.5 (12.2–13.4) g/dL in the control group; t (54) = −0.897, p = 0.374). Interestingly, there was no concurrent upregulation of TfR1 (M = 0.7 ± 1.2 versus 0.2 ± 0.4 for EM, t (54) = 2.552, p = 0.014), responsible for iron uptake into cells. Our empirical findings provide support for the involvement of ferroptosis in the context of endometriosis. However, variances in expression patterns within stromal and epithelial cellular subsets call for further in-depth investigations. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Endometriosis)
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14 pages, 5848 KiB  
Article
Estetrol Inhibits Endometriosis Development in an In Vivo Murine Model
by Ana Sofia Zabala, Rocío Ayelem Conforti, María Belén Delsouc, Verónica Filippa, Maria Magdalena Montt-Guevara, Andrea Giannini, Tommaso Simoncini, Sandra Silvina Vallcaneras and Marilina Casais
Biomolecules 2024, 14(5), 580; https://doi.org/10.3390/biom14050580 - 15 May 2024
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Abstract
Endometriosis is characterized by the growth of endometrial-like tissue outside the uterus, and it is associated with alterations in the expression of hormone receptors and inflammation. Estetrol (E4) is a weak estrogen that recently has been approved for contraception. We evaluated [...] Read more.
Endometriosis is characterized by the growth of endometrial-like tissue outside the uterus, and it is associated with alterations in the expression of hormone receptors and inflammation. Estetrol (E4) is a weak estrogen that recently has been approved for contraception. We evaluated the effect of E4 on the growth of endometriotic-like lesions and the expression of TNF-α, estrogen receptors (ERs), and progesterone receptors (PRs) in an in vivo murine model. Endometriosis was induced surgically in female C57BL/6 mice. E4 was delivered via Alzet pump (3 mg/kg/day) from the 15th postoperative day for 4 weeks. E4 significantly reduced the volume (p < 0.001) and weight (p < 0.05) of ectopic lesions. Histologically, E4 did not affect cell proliferation (PCNA immunohistochemistry) but it did increase cell apoptosis (TUNEL assay) (p < 0.05). Furthermore, it modulated oxidative stress (SOD, CAT, and GPX activity, p < 0.05) and increased lipid peroxidation (TBARS/MDA, p < 0.01). Molecular analysis showed mRNA (RT-qPCR) and protein (ELISA) expression of TNF-α decreased (p < 0.05) and mRNA expression of Esr2 reduced (p < 0.05), in contrast with the increased expression of Esr1 (p < 0.01) and Pgr (p < 0.05). The present study demonstrates for the first time that E4 limited the development and progression of endometriosis in vivo. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Endometriosis)
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Review

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17 pages, 2097 KiB  
Review
Regulated Cell Death in Endometriosis
by Erqing Huang, Xiaoli Wang and Lijuan Chen
Biomolecules 2024, 14(2), 142; https://doi.org/10.3390/biom14020142 - 23 Jan 2024
Cited by 4 | Viewed by 2143
Abstract
Regulated cell death (RCD) represents a distinct mode of cell demise, differing from accidental cell death (ACD), characterized by specific signaling cascades orchestrated by diverse biomolecules. The regular process of cell death plays a crucial role in upholding internal homeostasis, acting as a [...] Read more.
Regulated cell death (RCD) represents a distinct mode of cell demise, differing from accidental cell death (ACD), characterized by specific signaling cascades orchestrated by diverse biomolecules. The regular process of cell death plays a crucial role in upholding internal homeostasis, acting as a safeguard against biological or chemical damage. Nonetheless, specific programmed cell deaths have the potential to activate an immune–inflammatory response, potentially contributing to diseases by enlisting immune cells and releasing pro-inflammatory factors. Endometriosis, a prevalent gynecological ailment, remains incompletely understood despite substantial progress in unraveling associated signaling pathways. Its complexity is intricately tied to the dysregulation of inflammatory immune responses, with various RCD processes such as apoptosis, autophagic cell death, pyroptosis, and ferroptosis implicated in its development. Notably, limited research explores the association between endometriosis and specific RCD pathways like pyroptosis and cuproptosis. The exploration of regulated cell death in the context of endometriosis holds tremendous potential for further advancements. This article thoroughly reviews the molecular mechanisms governed by regulated cell death and their implications for endometriosis. A comprehensive understanding of the regulated cell death mechanism in endometriosis has the potential to catalyze the development of promising therapeutic strategies and chart the course for future research directions in the field. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Endometriosis)
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13 pages, 631 KiB  
Review
The Extracellular Vesicle–Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis
by Xiaoxiao Gao, Han Gao, Wei Shao, Jiaqi Wang, Mingqing Li and Songping Liu
Biomolecules 2023, 13(9), 1376; https://doi.org/10.3390/biom13091376 - 12 Sep 2023
Cited by 7 | Viewed by 1664
Abstract
Endometriosis (EMs) is a common disease among women whose pathogenesis is still unclear, although there are various hypotheses. Recent studies have considered macrophages the key part of the immune system in developing EMs, inducing inflammation, the growth and invasion of the ectopic endometrium, [...] Read more.
Endometriosis (EMs) is a common disease among women whose pathogenesis is still unclear, although there are various hypotheses. Recent studies have considered macrophages the key part of the immune system in developing EMs, inducing inflammation, the growth and invasion of the ectopic endometrium, and angiogenesis. Extracellular vesicles (EVs) as novel intercellular vesicle traffic, can be secreted by many kinds of cells, including macrophages. By carrying long non-coding RNA (lncRNA), microRNA (miRNA), or other molecules, EVs can regulate the biological functions of macrophages in an autocrine and paracrine manner, including ectopic lesion growth, immune dysfunction, angiogenesis, and can further accelerate the progression of EMs. In this review, the interactions between macrophages and EVs for the pathogenesis of EMs are summarized. Notably, the regulatory pathways and molecular mechanisms of EVs secreted by macrophages during EMs are reviewed. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Endometriosis)
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