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Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies 3.0
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Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies 3.0

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 June 2024 | Viewed by 5013

Special Issue Editors

Prof. Dr. Saad Amer

E-Mail Website
Guest Editor
Division of Medical Science and Graduate Entry Medicine, School of Medicine, Royal Derby Hospital Centre, University of Nottingham, Room 4115, Derby DE22 3DT, UK
Interests: reproductive medicine; reproductive biology; ovarian pathophysiology; polycystic ovary syndrome (PCOS)
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Raheela N. Khan

E-Mail Website
Guest Editor
Division of Medical Science and Graduate Entry Medicine, School of Medicine, Royal Derby Hospital Centre, University of Nottingham, Room 4115, Derby DE22 3DT, UK
Interests: ovarian physiology; reproductive physiology; metabolomics; ion channels; pregnancy disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Polycystic ovarian syndrome (PCOS) is the most common ovarian endocrinopathy affecting women of reproductive age. It is frequently associated with distressing reproductive, metabolic and androgenic disorders, which negatively affect the quality of life and psychological wellbeing of women. PCOS is also associated with serious long-term morbidities such as diabetes and heart disease. Despite its high prevalence and negative impact on health, the underlying mechanisms of PCOS remain largely unknown. Recent evidence implicates androgen excess, hyperinsulinaemia and chronic low-grade adipose tissue inflammation in the pathogenesis of PCOS. Currently, the management of PCOS only targets the presenting symptoms with no curative therapy, owing to an incomplete understanding of its underlying mechanisms. This Special Issue focuses on the molecular mechanisms that contribute to the development of PCOS. The Special Issue will also cover research that investigates new therapeutics targeting the roots of PCOS.

As volumes 1 and 2 of Special Issue “Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies” are successful, we reopen this Special Issue again. This third Special Issue, “Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies 3.0”, welcomes original manuscripts and review articles that address this hot topic.

Prof. Dr. Saad Amer
Prof. Dr. Raheela N. Khan
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • polycystic ovary syndrome
  • ovarian steroidogenesis
  • adipose tissue steroidogenesis
  • excess androgen synthesis
  • insulin resistance
  • theca cell dysfunction
  • chronic inflammation
  • insulin sensitizing agents

Published Papers (2 papers)

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Review

17 pages, 865 KiB  
Review
Polycystic Ovary Syndrome and Oxidative Stress—From Bench to Bedside
by Natalia Zeber-Lubecka, Michał Ciebiera and Ewa E. Hennig
Int. J. Mol. Sci. 2023, 24(18), 14126; https://doi.org/10.3390/ijms241814126 - 15 Sep 2023
Cited by 6 | Viewed by 2682
Abstract
Oxidative stress (OS) is a condition that occurs as a result of an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify and neutralize them. It can play a role in a variety of reproductive system conditions, [...] Read more.
Oxidative stress (OS) is a condition that occurs as a result of an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify and neutralize them. It can play a role in a variety of reproductive system conditions, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia, and infertility. In this review, we briefly discuss the links between oxidative stress and PCOS. Mitochondrial mutations may lead to impaired oxidative phosphorylation (OXPHOS), decreased adenosine triphosphate (ATP) production, and an increased production of ROS. These functional consequences may contribute to the metabolic and hormonal dysregulation observed in PCOS. Studies have shown that OS negatively affects ovarian follicles and disrupts normal follicular development and maturation. Excessive ROS may damage oocytes and granulosa cells within the follicles, impairing their quality and compromising fertility. Impaired OXPHOS and mitochondrial dysfunction may contribute to insulin resistance (IR) by disrupting insulin signaling pathways and impairing glucose metabolism. Due to dysfunctional OXPHOS, reduced ATP production, may hinder insulin-stimulated glucose uptake, leading to IR. Hyperandrogenism promotes inflammation and IR, both of which can increase the production of ROS and lead to OS. A detrimental feedback loop ensues as IR escalates, causing elevated insulin levels that exacerbate OS. Exploring the relations between OS and PCOS is crucial to fully understand the role of OS in the pathophysiology of PCOS and to develop effective treatment strategies to improve the quality of life of women affected by this condition. The role of antioxidants as potential therapies is also discussed. Full article
(This article belongs to the Special Issue Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies 3.0)
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22 pages, 3076 KiB  
Review
The Role of NLRP3 Inflammasome in Obesity and PCOS—A Systematic Review and Meta-Analysis
by Salih Atalah Alenezi, Raheela Khan, Lindsay Snell, Shaimaa Aboeldalyl and Saad Amer
Int. J. Mol. Sci. 2023, 24(13), 10976; https://doi.org/10.3390/ijms241310976 - 01 Jul 2023
Cited by 3 | Viewed by 1820
Abstract
Inflammasomes have recently been implicated in the pathogenesis of several chronic inflammatory disorders, such as diabetes and obesity. The aim of this meta-analysis was to investigate the possible role of the NLRP3 inflammasome in obesity and polycystic ovarian syndrome (PCOS). A comprehensive search [...] Read more.
Inflammasomes have recently been implicated in the pathogenesis of several chronic inflammatory disorders, such as diabetes and obesity. The aim of this meta-analysis was to investigate the possible role of the NLRP3 inflammasome in obesity and polycystic ovarian syndrome (PCOS). A comprehensive search of electronic databases was conducted to identify studies investigating NLRP3 its related components (Caspase 1, ASC and IL-1β) in adipose tissue and/or blood from obese individuals compared to non-obese controls. Another search was conducted for studies investigating NLRP3 in PCOS women and animal models. The ssearched databases included Medline, EMBASE, Cochrane Library, PubMed, Clinicaltrials.gov, the EU Clinical Trials Register and the WHO International Clinical Trials Register. The quality and risk of bias for the included articles were assessed using the modified Newcastle–Ottawa scale. Data were extracted and pooled using RevMan software for the calculation of the standardized mean difference (SMD) and 95% confidence interval (CI). Twelve eligible studies were included in the obesity systematic review and nine in the PCOS review. Of the obesity studies, nine (n = 270) were included in the meta-analysis, which showed a significantly higher adipose tissue NLRP3 gene expression in obese (n = 186) versus non-obese (n = 84) participants (SMD 1.07; 95% CI, 0.27, 1.87). Pooled analysis of adipose tissue IL-1β data from four studies showed significantly higher IL-1β gene expression levels in adipose tissue from 88 obese participants versus 39 non-obese controls (SMD 0.56; 95% CI, 0.13, 0.99). Meta-analysis of adipose tissue ASC data from four studies showed a significantly higher level in obese (n = 109) versus non-obese (n = 42) individuals (SMD 0.91, 95% CI, 0.30, 1.52). Of the nine PCOS articles, three were human (n = 185) and six were animal studies utilizing PCOS rat/mouse models. All studies apart from one article consistently showed upregulated NLRP3 and its components in PCOS women and animal models. In conclusion, obesity and PCOS seem to be associated with upregulated expression of NLRP3 inflammasome components. Further research is required to validate these findings and to elucidate the role of NLRP3 in obesity and PCOS. Full article
(This article belongs to the Special Issue Polycystic Ovary Syndrome: From Molecular Mechanisms to Therapies 3.0)
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