LAUSR

INTRODUCTION Many women of premenopausal age suffer from uterine leiomyomas, which are benign tumors of the uterus. Despite the high prevalence of uterine leiomyomas underlying pathogenesis mechanisms are not fully elucidated. Early data showed a positive correlation between increased levels of adipose tissue and leiomyomas prevalence. Adipose tissue cells-adipocytes can play a potential role in leiomyomas formation by producing and secreting adipokines. AIM The aim of this study is to summarize the current knowledge on the potential relation between adipokines and leiomyomas basing on current data analyze, and justify future research directions. METHODOLOGY This review is based on pertinent articles searched using PubMed, encompassing all available literature. The key search words were as follows: adipokines, leiomyoma, TNFα, leptin, adiponectin, visfatin, resistin, omentin, lipocalin, apelin, adipsin, chemerin. Time was not an exclusion criterium due to few available studies on this subject. SUMMARY The results of the studies are inconclusive, but the vast majority indicates a significant connection between the adipokines and the leiomyomas. According to the majority of studies, TNFα contributes to the development of leiomyomas by inhibiting apoptosis, increasing migration of leiomyomas, and increasing fibrosis of leiomyomas. Most of the studies on the effects of leptin also indicate the relation between leptin and leiomyomas development. In the case of adiponectin released from mast cells' granularity, it is possible that adiponectin increases angiogenesis in leiomyomas. Under physiological conditions, adiponectin has the potential to inhibit the development of leiomyomas. The authors suggested that adiponectin affects leiomyomas via an insulin-dependent pathway or via an estrogen-dependent pathway. Most probably leptin contributes to the formation of myomas and adiponectin prevents this. More research is needed to understand better the influence of these molecules on the pathogenesis of leiomyomas.