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, Sripriya Vennamaneni
2024 · doi:10.5281/zenodo.14292091 · W6968148421
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-12 ⓘ

This study found that severe endometriosis involves epithelial-mesenchymal transition, stem cell marker expression, and decreased mitochondrial oxidative phosphorylation gene expression compared to mild endometriosis and control samples.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text ⓘ

This study investigated mitochondrial oxidative phosphorylation dysfunction and how it may relate to epithelial–mesenchymal transition (EMT) in endometriosis using endometrial biopsies from women with severe endometriosis, women with mild endometriosis, and healthy controls, with analyses including cell viability, flow-cytometry-based immunophenotypic enrichment, and gene expression by real-time quantitative PCR. The authors found significantly decreased expression of OXPHOS genes and key regulators of mitochondrial dynamics/mitophagy (DRP1, Pink1, Parkin), alongside reduced E-cadherin expression in severe cases compared with mild and control groups. In parallel, severe endometriosis showed enhanced expression of mesenchymal stem cell markers (CD73, CD90, CD105), N-cadherin, and EMT- and hypoxia-related factors (HIF-1α, TWIST, SNAIL, SLUG). This paper provides a mechanistic association between mitochondrial dysfunction and EMT markers, but it does not address functional causality beyond gene expression and related assays, so validation is needed. This paper is centrally about endometriosis — specifically, the link between mitochondrial oxidative phosphorylation dysfunction and EMT-associated gene changes in severe endometriosis.

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Abstract

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.
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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. Files 32209-M no Q2 accepted file(Roya).pdf Files (1.5 MB) | Name | Size | Download all | |---|---|---| | md5:8d9b712927684f437d2ba4334d90bbc6 | 1.5 MB | Preview Download |

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