Abstract
Endometriosis is an estrogen-dependent chronic inflammatory condition that affects women in their reproductive period and is associated with pelvic pain and infertility. Oxidative stress (OS) occurs when reactive oxygen stress (ROS) and anti-oxidants are in imbalance. OS is a potential factor involved in the pathophysiology of endometriosis. Iron-induced ROS may trigger a chain of events resulting in the development and progression of endometriosis. Endogenous ROS are correlated with increased cellular proliferation and ERK1/2 activation in human endometriotic cells. An oxidative environment leads to stimulation of the ERK and PI3K/AKT/mTOR signaling pathways that facilitate endometriotic lesion progression through adhesion, angiogenesis, and proliferation. OS is also known to be involved in epigenetic mechanisms in endometriosis. We summarize the recent knowledge in our understanding of the role of oxidative stress in the pathogenesis of endometriosis.
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