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MMSCs from normal (MYON) and at\u2010risk (MYOF) uterine tissues were cultured in 3D organoids and treated with 1.6\u2009\u03bcM MEHHP for 48\u2009h. Functional assays investigated cell viability, apoptosis, and mitochondrial activity, whereas RT\u2010PCR, immunohistochemistry (IHC), and RNA sequencing evaluated markers of proliferation, apoptosis, extracellular matrix (ECM), and oxidative stress (OS). Cytokines and growth factors secretion were analyzed using a multiplex ELISA. Results showed that MEHHP exposure significantly increased cell viability and inhibited apoptosis in MYOF compared to MYON organoids. Proliferation markers (PCNA, Ki67), anti\u2010apoptotic markers (BCL2\/BAX ratio), and ECM markers (fibronectin and COL1A1) were significantly upregulated, whereas pro\u2010apoptotic markers (Caspase\u20103) were downregulated in MYOF organoids. MEHHP\u2010treated MYOF organoids exhibited elevated secretion of pro\u2010inflammatory cytokines (e.g., TNF\u2010\u03b1, IL\u20106, IL\u20108) and growth factors (e.g., PDGF, VEGF, TGF\u03b21), indicative of impaired tissue repair and fibrosis. RNA sequencing identified increased OS in MYOF organoids, validated by differential expression of genes such as CA9 and GPX3. Mitochondrial analysis revealed enhanced oxidative phosphorylation (OXPHOS) and elevated oxygen consumption rates, implicating mitochondrial dysfunction as a driver of cytokine release and UF pathogenesis. In conclusion, MEHHP was shown to promote the transformation of MYOF organoids into a UF phenotype by driving proliferation, inhibiting apoptosis, and inducing cytokine\u2010mediated inflammation via mitochondrial dysfunction. These findings related to MYOF\u2010specific effects, as compared to MYON, emphasize that these differences are statistically significant and relevant to UF risk. It can shed insight on how phthalates exposures may impact UF pathogenesis and provide a basis for exploring targeted therapeutic strategies.<\/jats:p>","DOI":"10.1002\/tox.70046","type":"journal-article","created":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T19:24:43Z","timestamp":1769973883000},"page":"975-997","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Phthalate Metabolite, Mono(2\u2010Ethyl\u20105\u2010Hydroxyhexyl) Phthalate (\n                    <scp>MEHHP<\/scp>\n                    ), Promotes Uterine\u2010Fibroid\u2013Associated Phenotypes in Myometrial Stem Cell\u2010Derived\n                    <scp>3D<\/scp>\n                    Organoids"],"prefix":"10.1002","volume":"41","author":[{"given":"Somayeh","family":"Vafaei","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Chicago  Chicago Illinois USA"},{"name":"Oncopathology Research Center, Iran 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