Molecular Characterization of Ovarian Endometriosis in Saudi Arabian Women: Insights into Inflammatory, Autophagic, and Epigenetic Dysregulation

Saber Nahdi, Maria Arafah, Felice Petraglia, Maroua Jalouli, Abdullah Alamri, Mohammad Alanazi, Md Ataur Rahman, Saleh Alwasel, Abdel Halim Harrath
In: International Journal of Molecular Sciences · 2026 · vol. 27(10) , pp. 4598 · doi:10.3390/ijms27104598 · PMID:42196574 · W7161753874
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated ovarian endometriosis in Saudi Arabian women, revealing stromal fibrosis, chronic inflammation, altered gene expression, a post-transcriptional paradox in IL-6, increased autophagy, and epigenetic dysregulation involving DNMT3B and H3.1.

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Abstract

Ovarian endometriosis (OE) is a chronic, inflammatory gynecological disorder associated with sterility and an elevated risk of ovarian cancer. Despite its high prevalence, the complex molecular mechanisms governing OE pathogenesis remain poorly investigated. We conducted a comprehensive histopathological and molecular investigation of OE in a cohort of 188 Saudi women (88 patients with OE and 100 healthy controls) using histopathological, qRT-PCR, immunostaining, and Western blot techniques. Histopathological analysis confirmed significant stromal fibrosis and chronic inflammation in endometriotic lesions. Gene expression profiling revealed a pro-proliferative, anti-apoptotic signature, marked by the upregulation of PTTG1 and the downregulation of TNFRSF10D, CDK4, and CDKN1A. Interestingly, we identified a post-transcriptional regulatory paradox in the inflammatory response: while IL-6 mRNA was significantly upregulated, its corresponding protein level was downregulated, suggesting a novel, tightly controlled mechanism to limit excessive local inflammation. Besides the increased autophagic activity and decreased Ubiquitin mRNA levels, epigenetic dysregulation was prominent, characterized by the upregulation of DNA methyltransferase DNMT3B and the downregulation of the histone variant H3.1. These findings elucidate novel molecular pathways underlying OE pathogenesis as evidenced by a post-transcriptional paradox in IL-6 expression, and uncover key dysregulations spanning cell proliferation, apoptosis, inflammation, autophagy, and epigenetic regulation.

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endometriosis

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