The role of mitogen-activated protein kinase signaling pathway in endometriosis

摘要

Aim Endometriosis is an estrogen-dependent chronic inflammatory condition which causes pain, infertility, and predisposition for ovarian cancer. Endometriosis generates a unique microenvironment for survivability of endometriotic lesions which includes cell proliferation, differentiation, migration, and apoptosis. For these cellular activities, cascading activations of intracellular kinases are needed. Many kinase signaling pathways, IKK beta/NK-kappa B pathway, PI3K/AKT/mTOR, and the mitogen-activated protein kinase (MAPK) pathways (ERK1/2, p38, and JNK), are activated in endometriosis. In this review, we focus on the role of MAPK pathways in endometriosis.