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Abstract UFs represent a significant global health problem. They are considered as a significant cause of morbidity for women of reproductive age leading to significant distress and negatively impacting women’s quality of life and work productivity (Fischer et al., 2021 and Tinelli et al., 2021). Moreover, the UF morbidity is underscored by being the main reason behind various surgeries, mainly hysterectomy (Ciebiera et al., 2018) Many different risk factors have been associated with the development of UFs including obesity (Okolo, 2008 and Templeman et al., 2009), however, definitive conclusions concerning the possible correlation between obesity and UFs are still lacking. While these widespread tumors have been the subject of basic and translational studies for decades (Jayes et al., 2019), UFs molecular pathobiology remains elusive, and as a result current medical treatment options are limited The present study was designed to investigate the role of FAP, a marker of fibroblast activation as well as the role of autophagy dysfunction, inflammatory cytokines and oxidative stress in the pathogenesis of UF. The study also aimed at assessing the link between fibroblast activation and autophagy suggested through the PI3K/AKT signaling pathway. The current study was performed on 35 pre-menopausal women (age ˂ 50 years) enrolled to undergo hysterectomy for symptomatic UF. The average age of the patients was 44.06 ± 2.87 years (range, 39–49 years). Patients were further divided according to BMI into non-obese (BMI ≤30 kg/m2) and obese (BMI >30 kg/m2). Fifteen patients were non-obese and twenty patients were obese. Tissue samples were collected from fibroids and adjacent myometrium (2 cm away from fibroid lesions). The location of fibroids (single or multiple) was predominantly intramural and their size range was 4–6 cm in diameter. UFs were previously diagnosed by ultrasonography, and the diagnosis was further confirmed by histopathological evaluation of surgical specimens. |