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REVIEW article

Front. Med.
Sec. Obstetrics and Gynecology
Volume 11 - 2024 | doi: 10.3389/fmed.2024.1425691
This article is part of the Research Topic Endometriosis: Updates on the Etiology, Pathophysiology, Measurements and Therapeutics View all 4 articles

The Vicious Cycle of Chronic Endometriosis and Depression-An Immunological and Physiological Perspective Running head: Vicious cycle of endometriosis and depression

Provisionally accepted
Subuhi Sherwani Subuhi Sherwani 1*Mohd Wajid A. Khan Mohd Wajid A. Khan 2*Saravanan Rajendrasozhan Saravanan Rajendrasozhan 3Khalid Al-Motair Khalid Al-Motair 2Qayyum Hussain Qayyum Hussain 4Wahid Ali Khan Wahid Ali Khan 5
  • 1 Department of Biology, College of Sciences, University of Hail, Hail, Saudi Arabia
  • 2 Medical and Diagnostic Research Centre, University of Hail, Hail,, Saudi Arabia
  • 3 Department of Chemistry, College of Sciences, University of Hail, Hail, Saudi Arabia
  • 4 Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
  • 5 Department of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, Saudi Arabia

The final, formatted version of the article will be published soon.

    Endometriosis is a chronic, estrogen-dependent, proinflammatory disease that can cause various dysfunctions. The main clinical manifestations of endometriosis include chronic pelvic pain and impaired fertility. Endometriosis The disease is characterized by a spectrum of dysfunctions spanning hormonal signaling, inflammation, immune dysregulation, angiogenesis, neurogenic inflammation, epigenetic alterations, and tissue remodeling. Dysregulated hormonal signaling, particularly involving estrogen and progesterone, drives abnormal growth and survival of endometrial-like tissue outside the uterus. Chronic inflammation, marked by immune cell infiltration and inflammatory mediator secretion, perpetuates tissue damage and pain. Altered immune function, impaired ectopic tissue clearance, and dysregulated cytokine production contribute to immune dysregulation. Enhanced angiogenesis driven by pro-angiogenic factors promotes lesion growth and survival. Epigenetic modifications influence gene expression patterns such as e.g. HSD11B1 gene, affecting disease pathogenesis. Endometriosis related changes and infertility lead to depression in diagnosed women diagnosed with endometriosis. Depression changes lifestyle and induces physiological and immunological changes. A higher rate of depression and anxiety has been reported found in women diagnosed with endometriosis diagnosed women, unleashing physiological, clinical and immune imbalances which further accelerate chronic endometriosis or vice versa. Thus, both endometriosis and depression are concomitantly develop part of a vicious cycle and that enhance the disease complications. A multidimensional treatment strategy is needed which can cater for both endometrial disease treatment and depression and anxiety disorders related counselling and treatment.

    Keywords: estrogen, Endometriosis, estrogen receptor, Inflammation, Depression, Immune imbalance

    Received: 30 Apr 2024; Accepted: 12 Aug 2024.

    Copyright: © 2024 Sherwani, Khan, Rajendrasozhan, Al-Motair, Hussain and Khan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Subuhi Sherwani, Department of Biology, College of Sciences, University of Hail, Hail, Saudi Arabia
    Mohd Wajid A. Khan, Medical and Diagnostic Research Centre, University of Hail, Hail,, Saudi Arabia

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.