ArticleJournal of translational medicine2024
Multi-omics integration highlights the role of ubiquitination in endometriosis fibrosis.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Endometriosis-associated infertility: Multi-omics insights into pathogenesis and precision therapeutics.Frontiers in endocrinology · 2025Pooled it
- Exosomal miR-21-5p from ectopic endometrial stromal cells drives fibrosis progression in endometriosis through direct VHL targeting.Human cell · 2026Article
- Piezo1 mediates hypoxia-induced endometriosis fibrosis via the mtDNA -dependent cGAS-STING pathway.Journal of translational medicine · 2026Article
- Advances in multi-omics and aging clock research for female reproductive health and aging.MedScience · 2026Review
- The therapeutic potential of pirfenidone in alleviating fibrosis and restoring ovarian function in a novel ovarian endometriosis mouse model.Journal of translational medicine · 2026Article
- Early modulation of autophagy-associated markers in murine adenomyosis and selective persistence in human stromal lesions.Frontiers in endocrinology · 2026Article
- Identification and Validation of a Four-Gene Signature as a Novel Potential Diagnostic Biomarker Panel for Endometriosis: Causal and Mechanistic Insights from Mendelian Randomization and Bioinformatics.International journal of women's health · 2026Article
- SIRT7 drives energy metabolic shifts in endometriosis via interaction with TUFM and Rhoa/Rock/Akt pathway activation.Cellular and molecular life sciences : CMLS · 2025Article
- SAT1 promotes the progression of OA by regulating TRIM33-mediated p53 acetylation to enhance ferroptosis.PloS one · 2025Article
- Single-Cell Transcriptomic Analysis Highlights the Impact of NFKB2-Mediated MIF-CD44 Signaling Axis in Endometrioid Endometrial Cancer.International journal of women's health · 2025Article
- Gut microbiota in dysmenorrhea: causal evidence from Mendelian randomization and microbial-targeted intervention validation.Frontiers in microbiology · 2025Article
- Elevated MMP-9, Survivin, TGB1 and Downregulated Tissue Inhibitor of TIMP-1, Caspase-3 Activities are Independent of the Low Levels miR-183 in Endometriosis.International journal of women's health · 2024Article
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10 authors.
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Abstract
backgroundEndometriosis, characterized by the presence of active endometrial-like tissues outside the uterus, causes symptoms like dysmenorrhea and infertility due to the fibrosis of endometrial cells, which involves excessive deposition of extracellular matrix (ECM) proteins. Ubiquitination, an important post-transcriptional modification, regulates various biological processes in human diseases. However, its role in the fibrosis process in endometriosis remains unclear.
methodsWe employed multi-omics approaches on two cohorts of endometriosis patients with 39 samples. GO terms and KEGG pathways enrichment analyses were used to investigate the functional changes involved in endometriosis. Pearson's correlation coefficient analysis was conducted to explore the relationship between global proteome and ubiquitylome in endometriosis. The protein expression levels of ubiquitin-, fibrosis-related proteins, and E3 ubiquitin-protein ligase TRIM33 were validated via Western blot. Transfecting human endometrial stroma cells (hESCs) with TRIM33 small interfering RNA (siRNA) in vitro to explore how TRIM33 affects fibrosis-related proteins.
resultsIntegration of proteomics and transcriptomics showed genes with concurrent change of both mRNA and protein level which involved in ECM production in ectopic endometria. Ubiquitylomics distinguished 1647 and 1698 ubiquitinated lysine sites in the ectopic (EC) group compared to the normal (NC) and eutopic (EU) groups, respectively. Further multi-omics integration highlighted the essential role of ubiquitination in key fibrosis regulators in endometriosis. Correlation analysis between proteome and ubiquitylome showed correlation coefficients of 0.32 and 0.36 for ubiquitinated fibrosis proteins in EC/NC and EC/EU groups, respectively, indicating positive regulation of fibrosis-related protein expression by ubiquitination in ectopic lesions. We identified ubiquitination in 41 pivotal proteins within the fibrosis-related pathway of endometriosis. Finally, the elevated expression of TGFBR1/α-SMA/FAP/FN1/Collagen1 proteins in EC tissues were validated across independent samples. More importantly, we demonstrated that both the mRNA and protein levels of TRIM33 were reduced in endometriotic tissues. Knockdown of TRIM33 promoted TGFBR1/p-SMAD2/α-SMA/FN1 protein expressions in hESCs but did not significantly affect Collagen1/FAP levels, suggesting its inhibitory effect on fibrosis in vitro.
conclusionsThis study, employing multi-omics approaches, provides novel insights into endometriosis ubiquitination profiles and reveals aberrant expression of the E3 ubiquitin ligase TRIM33 in endometriotic tissues, emphasizing their critical involvement in fibrosis pathogenesis and potential therapeutic targets.
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