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: 30 September 2024 | Viewed by 2879

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

Manuscript Submission Information

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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

Published Papers (2 papers)

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Review

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
Viewed by 1298
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 3 | Viewed by 1243
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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