The role of epithelial-mesenchymal transition in the pathogenesis of various diseases: A review

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Abstract

Epithelial-mesenchymal transition (EMT) is a cellular process in which epithelial cells acquire the phenotype and properties of mesenchymal cells. This process plays a large and important role in the progression of various diseases, in the launch of trigger mechanisms at various stages of development, both in men and women, of different age categories. The conducted analysis of literary data allows us to conclude that the triggering factors of EMT in the pathogenesis of various diseases are similar. The impact on the molecular biological targets of EMT will prevent the formation of diseases at early stages. This fact will contribute to the search for targeted drugs for the treatment of such patients.

About the authors

Mariam A. Vardanyan

Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology

Author for correspondence.
Email: mv132013@mail.ru
ORCID iD: 0009-0002-4619-1431

Graduate Student

Russian Federation, Moscow

Ellina I. Pilyugina

Guta-Clinic

Email: ellinapiliugina@gmail.com
ORCID iD: 0009-0003-5440-7674

Surgeon

Russian Federation, Moscow

Alina S. Badlaeva

Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology

Email: a_badlaeva@oparina4.ru
ORCID iD: 0000-0001-5223-9767

Cand. Sci. (Med.)

Russian Federation, Moscow

Vladimir D. Chuprynin

Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology

Email: v_chuprynin@oparina4.ru
ORCID iD: 0000-0002-2997-9019

Cand. Sci. (Med.)

Russian Federation, Moscow

Natalya A. Buralkina

Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology

Email: natalyaburalkina@yandex.ru
ORCID iD: 0000-0001-5109-6725

D. Sci. (Med.)

Russian Federation, Moscow

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2. Fig. 1. Cellular changes within the EMT program: a – rupture of cell contacts (desmosomes). Destruction of polarity complexes and loss of cell polarity. Decreased expression of epithelial genes and activation of expression of mesenchymal genes; b – reorganization of the structure of cellular actin and acquisition of motility and the ability to invade (formation of filopodia, matrix metalloproteases) [41].

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