INVESTIGATING INFECTION'S ROLE AS A CONTRIBUTING FACTOR IN THE GENETIC AND EPIGENETIC MECHANISMS OF ENDOMETRIOSIS: A NARRATIVE REVIEW.

Archana Jha
In: sjc · 2024 · doi:10.51168/sjhrafrica.v5i3.1057 · W4399545170
dissertation OA: gold CC0
🔓 Open OA copy Full text JSON View on OpenAlex View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-13 ⓘ

This review examines how infections may interact with genetic predispositions and epigenetic modifications, influencing the development and progression of endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-13 · read from full text ⓘ

This narrative review examines evidence linking infections to the genetic and epigenetic mechanisms proposed in endometriosis, focusing on how host immune responses and inflammation-related gene regulation may be shaped by infectious exposures. It highlights that genetic predispositions for endometriosis have been associated with enhanced immune responses to infections, including immune-system and inflammatory gene variants such as Toll-like receptor 4 (TLR4), and it describes how infections may drive epigenetic modifications that alter gene expression relevant to inflammation, immune surveillance, and tissue repair. A key limitation is that, as a narrative review, it does not present a systematic, quantified synthesis of the underlying studies. Relevance to endometriosis: the paper is centrally about endometriosis, specifically linking infections to genetic predispositions and epigenetic modifications involved in its development and progression.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a chronic gynecological condition, characterized by the presence of endometrial-like tissue outside the uterus. It is associated with symptoms such as pelvic pain, dysmenorrhea, and infertility, significantly impacting women's quality of life. Despite its prevalence, the pathophysiology of endometriosis is not fully understood, with genetic, epigenetic, environmental, immunological, and hormonal factors all playing roles in its development. This review aims to systematically examine the evidence linking infections to the genetic and epigenetic mechanisms of endometriosis, highlighting how these interactions may contribute to the disease's development and progression. Recent research has identified a connection between genetic predispositions to endometriosis and an enhanced immune response to infections. Specific genetic markers associated with an increased risk of endometriosis have also been linked to heightened immune reactions to infectious agents, suggesting a complex interplay between endometriosis and infections. Variations in genes regulating the immune system and inflammatory processes, such as the Toll-like receptor 4 (TLR4), have been implicated in both endometriosis and the body's response to infections. Furthermore, infections can induce epigenetic changes that may influence the development and severity of endometriosis by altering gene expression related to inflammation, immune surveillance, and tissue repair. Understanding the relationship between infections, genetic predispositions, and epigenetic modifications in endometriosis opens new avenues for research into targeted therapies. Addressing the underlying genetic and immunological factors contributing to endometriosis could lead to more effective treatment strategies, potentially improving the quality of life for those affected by the condition. Clinicians should consider the potential role of infections in the exacerbation of endometriosis symptoms and the importance of comprehensive patient evaluations to identify and treat any concurrent infections. Future therapeutic strategies should also explore anti-inflammatory therapies and preventive measures against pathogens known to influence endometriosis progression.
Full text 2,718 characters · extracted from oa-doi-fallback · click to expand
INVESTIGATING INFECTION'S ROLE AS A CONTRIBUTING FACTOR IN THE GENETIC AND EPIGENETIC MECHANISMS OF ENDOMETRIOSIS: A NARRATIVE REVIEW. DOI: https://doi.org/10.51168/sjhrafrica.v5i3.1057Keywords: Endometriosis, Infections, Genetic Predispositions, Epigenetic ModificationsAbstract Endometriosis is a chronic gynecological condition, characterized by the presence of endometrial-like tissue outside the uterus. It is associated with symptoms such as pelvic pain, dysmenorrhea, and infertility, significantly impacting women's quality of life. Despite its prevalence, the pathophysiology of endometriosis is not fully understood, with genetic, epigenetic, environmental, immunological, and hormonal factors all playing roles in its development. This review aims to systematically examine the evidence linking infections to the genetic and epigenetic mechanisms of endometriosis, highlighting how these interactions may contribute to the disease's development and progression. Recent research has identified a connection between genetic predispositions to endometriosis and an enhanced immune response to infections. Specific genetic markers associated with an increased risk of endometriosis have also been linked to heightened immune reactions to infectious agents, suggesting a complex interplay between endometriosis and infections. Variations in genes regulating the immune system and inflammatory processes, such as the Toll-like receptor 4 (TLR4), have been implicated in both endometriosis and the body's response to infections. Furthermore, infections can induce epigenetic changes that may influence the development and severity of endometriosis by altering gene expression related to inflammation, immune surveillance, and tissue repair. Understanding the relationship between infections, genetic predispositions, and epigenetic modifications in endometriosis opens new avenues for research into targeted therapies. Addressing the underlying genetic and immunological factors contributing to endometriosis could lead to more effective treatment strategies, potentially improving the quality of life for those affected by the condition. Clinicians should consider the potential role of infections in the exacerbation of endometriosis symptoms and the importance of comprehensive patient evaluations to identify and treat any concurrent infections. Future therapeutic strategies should also explore anti-inflammatory therapies and preventive measures against pathogens known to influence endometriosis progression. Downloads Published How to Cite Issue Section License Copyright (c) 2024 Archana Jha This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosisdysmenorrheainfertility

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (10)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK