Gynecology & Obstetrics
Open Access

Abstract

Impact of Mitochondrial Oxidative Phosphorylation Dysfunction in the Patient with Endometriosis

Roya Rozati*, Aleem Ahmed Khan, Wajeeda Tabasum, Salwa Sahar Azimi, Vikram Aiman Ayapati, Ayapati Gautam Mehdi, Nasaruddin Khaja, Krishnan Sivaraman and Sripriya Vennamaneni

Background: Endometriosis is a chronic inflammatory condition where the precise cause of endometriosis is still not unclear. Mitochondrial dysfunction has been reported in severe forms of endometriosis. However, the role of mitochondrial dynamics, mitophagy, and mitochondrial-related complexes in endometriosis and its relation with Epithelial-Mesenchymal Transition (EMT) is not clear.
Objective: Therefore, this study aims to elucidate the role of mitochondrial dysfunction and its relation with EMT in the pathogenesis of endometriosis.
Material and methods: At present, cell viability, immunophenotypic enrichment using flow cytometry, and gene expression by real-time quantitative PCR were carried out.
Results: A significant decrease in the expression of OXPHOS genes, DRP1, Pink-1, Parkin, and E-cadherin in endometrial biopsies collected from women with severe endometriosis compared to biopsies collected both from healthy women and women with mild endometriosis was noted. Enhanced expression of mesenchymal stem cell markers (CD73, CD90, and CD105), N-cadherin, hypoxia-inducible factor-1α, TWIST, SNAIL, and SLUG were severe endometrial forms compared to mild form and controls.
Conclusion: Our observations revealed the presence of EMT in severe forms of endometriosis, accompanied by the expression of MSC markers and strongly imply the role of EMT in the pathogenesis of endometriosis. Additional research endeavours are necessary to validate and build upon these discoveries, with the ultimate goal of enhancing care and outcomes for individuals afflicted by endometriosis.

Published Date: 2024-07-25; Received Date: 2024-07-03