17β-estradiol, acting through estrogen receptors α and β, plays a fundamental role in the regulation of Fallopian tube cell homeostasis and in the modulation of normal tubal physiological processes. Fluctuations in E2 levels also play crucial roles in the initiation or progression of numerous human diseases. Fallopian tube malfunction often results in tubal ectopic pregnancy, which is one cause of maternal morbidity and mortality in women. Several factors have been proposed to be associated with increased risk of tubal ectopic pregnancy, but whether these factors are the cause of, or are merely symptoms of, such pregnancies remains unresolved due to the lack of knowledge in regards to the mechanisms by which embryos inadvertently implant in the Fallopian tube. This review summarizes recent findings, including data from our own laboratory, on E2 metabolism and estrogen receptor (ER) subtype expression within the Fallopian tube in humans and rodents. This review also outlines several important, unresolved questions in the field that, once addressed, could offer important clues into how E2/ER signaling contributes to the pathology of tubal function. A better understanding of the specific functions of estrogen receptor subtypes in vivo, as well as of the mechanism and consequences of receptor subtype interactions is critical to understanding their respective roles in Fallopian tube physiology and in the pathophysiology and etiology of tubal ectopic pregnancy.
Keywords: 17β-estradiol; estrogen receptor subtypes; human; infertility; tubal ectopic pregnancy.