Objective: The objective of this study was to investigate whether or not there is a cellular response to hypoxic damage in cells of pelvic structures in women with POP (pelvic organ prolapse) and in those from the control group, as well as to analyze the mitochondrial function in the muscular layer of the vagina in woman with POP, and to compare it with the samples collected from the control group. Materials and Methods: The study included 120 subjects hospitalized at the Department of Gynecology and Obstetrics, University Hospital Center of Split. The subjects were divided into two groups. The POP group (60 subjects) consisted of patients who underwent vaginal hysterectomy due to POP. The control group (60 respondents) consisted of patients who underwent abdominal hysterectomy due to benign gynecological diseases. Mitochondrial function analysis was performed for 16 subjects (10 from the POP group and 6 from the control group). During the surgical procedure, tissue sampling was performed. Immunohistochemical methods were used to determine the positivity of the HIF-1α protein in vaginal cells, uterosacral ligaments and levator ani muscle. The Western blotting method was used to determine the status of five respiratory mitochondria complexes in the muscle layer of the vagina. Results: A higher number of HIF-1α positive stromal cells was found in the vaginal wall of women with POP in comparison with those from the control group (P <0.05), while there was no statistically significant increase in expression of HIF-1α in the uterosacral ligament or levator ani muscle of women with prolapse in comparison with those from the control group. A decreased expression of mitochondrial respiratory complex II was found in the vaginal wall of patients with POP in comparison with those from the control group (P <0.05). Conclusion: Results indicate the existence of hypoxic damage and dysfunctional mitochondrial oxidative capacity in women with POP in comparison with the control group, which might be of importance when it comes to clarifying POP etiopathogenesis.