Pathophysiological Changes in Early Endometriosis

Endometriosis is a common but complex gynecological disorder of unknown pathogenesis. It is characterized by ectopic growth of endometrial tissues. Based on Sampson’s classical implantation theory, retrograde menstruation, immune escape, adhesion, angiogenesis and growth of endometrial cells are essential milestones in the pathogenesis of endometriosis. The cellular communications of immune, endothelial and endometriotic cells during endometriosis development are mediated via cytokines and chemokines. Many specific cytokines in peritoneal fluid of patients with endometriosis are aberrant from normal women. However, it’s not clear at which stage of endometriosis these aberrant cytokines begin to change and owing to the limitation with human study the functions of these cytokines were only investigated in vitro. On the other hand, the onset of angiogenesis is initiated by oxidative stress due to cellular and tissue hypoxia, which is mainly coordinated by the hypoxiainducible factors (HIFs). HIFs stimulate VEGF transcription and activation in endometriosis lesions in acquiring new blood vessels for survival and growth. Monitoring inflammatory response, oxidative stress and angiogenesis in the endometriosis lesions is of vital importance in understanding the pathophysiological changes during early development of endometriosis.

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