Uterine fibroids: a look at the problem

Abstract

Despite scientific progress, there is currently no sigle opinion about the cause of the occurrence and recurrence of uterine fibroids, but due to the high level of molecular medicine, progress is being made in the hormonal and molecular genetic mechanisms of initiation, formation and growth of the fibroisds. The issue of pathogenetic treatment and prevention of recurrence of uterine fibroids in reproductive age remains relevant. The aims of the review. The aim of this review is to summarize current data about microRNA in biology of uterine leiomyoma (LM). This information can improve our understanding of the broad molecular interaction of signaling pathways in the formation of LM, and further maintaining epigenetic regulation as an important mechanism in the pathogenesis of uterine leiomyoma. In leiomyomas, the expression of a number of non-proteincoding genes is altered, such as microRNAs (miRNAs), which target genes that code protein. Material and research methods. Original and review articles, book chapters in the PubMed database related to the study of the pathogenesis of uterine fibroids in the period from 2004 to 2022 were found and analyzed. Results and discussions. Based on an analytical review of the literature, it becomes obvious that as evidence should be considered: 1. Abnormal myometrial and fibroid stem cells show an increased response to estrogen and progesterone exposure, stimulating processes such as cell proliferation, inhibition of apoptosis, and extracellular matrix (ECM) formation. 2. A number of tumor suppressor genes are abnormally hypermethylated in the LM when compared to normal myometrium, genes that form and regulate collagen, and a subset of estrogen receptor genes. 3. Multiple studies using microarray analysis or sequencing have demonstrated the existence of dysregulation of a number of protein-coding genes involved in cell proliferation and apoptosis, which are critical for the growth and progression of uterine fibroids. There are no reliable evidence base and do not provide an opportunity for practical application of clinically significant risk factors, the possibility of mathematical prediction of the growth of uterine fibroids in women of reproductive age. Data on the effect of the expression of a number of microRNAs on the growth of uterine fibroids in vivo are rather contradictory. The epigenetic processes of regulation and pathogenesis of the growth of leiofibromyomas in reproductive age have not been fully studied and substantiated. There are practically no data on predicting the growth of uterine fibroids in reproductive age, which will allow us to assess the risk of growth and determine further treatment tactics. Conclusion. Further work on the identification of specific genes, miRNAs, that are involved in the pathogenesis of LM may inspire the creation of new pathogenetic treatments. Such treatment is especially relevant for those groups of patients of reproductive age for whom surgical treatment may be ineffective. Targeted treatment can also prevent the recurrence of uterine fibroids, hence the need for repeat surgery.