Current knowledge on endometriosis etiology: A systematic review of literature

Objective: To review the mechanisms of endometriosis development, including those related to epigenetic mutations, cellular dysregulation, inflammatory processes, and oxidative stress. Methods: A systematic literature review regarding current aspects of endometriosis etiology, genesis and development was performed using the PubMed, Google Scholar, and eLibrary databases. Keywords included endometriosis, etiology, development, genesis, associations and mechanisms. A multilingual search was performed. Results: Several mechanisms underline the pathophysiological pathways for endometriosis development. Epigenetic mutations, external and internal influences, and chronic conditions have a significant impact on endometriosis development, survival and regulation. Several historically valid theories on endometriosis development were discussed, as well as updated findings. Conclusion: Despite recent advances, fundamental problems in understanding endometriosis remain unresolved. The identification of unknown circulating epithelial progenitors or stem cells that are responsible for epithelial growth in both the endometrium and endometriotic foci seems to be the next step in solving these questions. © 2021 Mikhaleva et al.

Authors
Mikhaleva L.M. 1 , Radzinsky V.E. 2 , Orazov M.R. 2 , Khovanskaya T.N.1 , Sorokina A.V. 1 , Mikhalev S.A.3 , Volkova S.V. 2 , Shustova V.B. 1 , Sinelnikov M.Y.1
Publisher
Dove Medical Press Ltd
Language
English
Pages
525-537
Status
Published
Volume
13
Year
2021
Organizations
  • 1 Laboratory of Clinical Morphology, Research Institute of Human Morphology, Moscow, Russian Federation
  • 2 Peoples’ Friendship University (RUDN), Moscow, Russian Federation
  • 3 Family Planning and Reproduction Center, Moscow, Russian Federation
Keywords
Endometriosis etiology; Endometriosis markers; Endometriosis progression; Genesis
Date of creation
16.12.2021
Date of change
16.12.2021
Short link
https://repository.rudn.ru/en/records/article/record/77196/
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