Advances in molecular mechanisms of pelvic organ prolapse (Review)

xlomafota13 shared this article with you from Inoreader Advances in molecular mechanisms of pelvic organ prolapse (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):1009. doi: 10.3892/etm.2021.10442. Epub 2021 Jul 15. ABSTRACT Pelvic organ prolapse (POP) is a common gynecological benign disease occurring in middle-aged and elderly females. Its incidence increases every year. To date, the majority of studies investigating its etiology have not evaluated the underlying molecular mechanisms, which has caused substantial difficulties in the prevention, treatment and prognosis of POP. In the present narrative review, recent research studies concerning the molecular mechanisms of POP were systematically reviewed and the advances were summarized. The association between the incidence of POP and the reduction of the extracellular matrix, activation of oxidative stress, genetic susceptibility, denervation of the pelvic floor and reduction of estrogen infiltration were explored. POP is mainly associated with damage of pelvic floor muscles and connective tissue, which are directl y caused by pregnancy and vaginal delivery. The majority of the molecular and genetic mutations associated with POP involve specific components of connective tissue synthesis and degradation. It is likely that macroscopic parameters, such as anatomy, lifestyle and reproductive factors, interact with microscopic parameters, such as physiology and genetics in the female pelvic floor, leading to POP. Additional research studies investigating the molecular mechanisms of POP should be performed, since they may aid public health strategies. In the present narrative review, a summary of these molecular mechanisms underlying the development of POP is provided. This included the relevant proteins and genes involved. On this basis, countermeasures were proposed. PMID:34345291 | PMC:PMC8311251 | DOI:10.3892/etm.2021.10442 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.