A Review of the Molecular Basis for Reduced Endometrial Receptivity in Uterine Fibroids and Polyps

Abstract

role of HOX genes and transforming growth factor β3, which are key markers of endometrial receptivity. Understanding the process by which fibroids and polyps reduce fertility is crucial to both improving implantation rates, and guiding future therapy options, which currently focuses upon surgical resection as optimal care (10, 11). Fibroids Fibroids, or leiomyomas, are typically benign, smooth muscle tumors arising from the myometrium, consisting of disorganized smooth muscle cells, vascular smooth muscle cells, fibroblasts, and fibroid-associated fibroblasts. Fibroids are the most common benign tumor of reproductive women, occurring in about 20%-50% of women (12). These lesions are broadly classified as either submucosal, intramural, or subserosal and their location and size has thus far been considered the major determinants of their symptomatology and burden of disease. The complete reproductive impact of fibroids remains an ongoing focus of research. Fibroids that deform or line the uterine cavity are thought to alter overlying endometrial receptivity and uterine peristalsis, and possibly obstruct sperm migration (12, 13). While it is widely accepted that cavity-distorting fibroids have reduced fertility outcomes, the role of asymptomatic and noncavity distorting fibroids-as well as those of small size-is still undetermined. A study of 119 women with asymptomatic intramural or subserosal fibroids <5 cm found no significant difference in live birth rates when matched to controls (14). Similarly, Yan et al (15) observed no gross difference in in vitro fertilization/intracytoplasmic sperm injection cycle success rates for women with or without fibroids, though a negative effect on delivery rate was noted for fibroids larger than 2.85 cm. However, the most comprehensive evidence remains 2 systematic reviews