Cellular Components Contributing to Fibrosis in Endometriosis: A Literature Review.


Journal

Journal of minimally invasive gynecology
ISSN: 1553-4669
Titre abrégé: J Minim Invasive Gynecol
Pays: United States
ID NLM: 101235322

Informations de publication

Date de publication:
02 2020
Historique:
received: 16 08 2019
revised: 31 10 2019
accepted: 21 11 2019
pubmed: 1 12 2019
medline: 29 8 2020
entrez: 1 12 2019
Statut: ppublish

Résumé

Endometriosis-related fibrosis represents a complex phenomenon with underlying mechanisms yet to be clarified. Fibrosis is consistently present in all disease forms and contributes to classic endometriosis-related symptoms of pain and infertility. The purpose of this literature review was to examine the role of various cellular populations and biologic mechanisms and signaling pathways in inducing fibrogenesis of endometriotic lesions. A search was performed through PubMed and MEDLINE for animal and human studies published in English in the last 23 years that examined fibrosis in superficial, ovarian, and deep infiltrating endometriosis. The main cell types found to be involved in the development of fibrosis were platelets, macrophages, ectopic endometrial cells, and sensory nerve fibers. Interactions among each of the cell types contribute to the production of fibrosis through the production of soluble factors, mostly transforming growth factor-β but also other cytokines and neuropeptides. Cell types known to be critical to the pathophysiology of endometriosis also contribute to fibrogenesis, thus supporting the theory that fibrosis is an inherent part of endometriosis.

Identifiants

pubmed: 31785417
pii: S1553-4650(19)31299-3
doi: 10.1016/j.jmig.2019.11.011
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

287-295

Informations de copyright

Copyright © 2019 AAGL. Published by Elsevier Inc. All rights reserved.

Auteurs

Paola Viganò (P)

Reproductive Sciences Lab, Division of Genetics and Cell Biology (Dr. Vigano). Electronic address: vigano.paola@hsr.it.

Jessica Ottolina (J)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

Ludovica Bartiromo (L)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

Giulia Bonavina (G)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

Matteo Schimberni (M)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

Roberta Villanacci (R)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

Massimo Candiani (M)

Gynecology/Obstetrics Unit (Drs. Ottolina, Bartiromo, Bonavina, Schimberni, Villanacci, and Candiani), San Raffaele Scientific Institute, Milan, Italy.

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Classifications MeSH