Abstract:

Endometriosis (EMs) is a common benign disease in women of childbearing age which seriously affects patients′ quality of life, and its incidence is increasing year by year. Autophagy is a kind of programmed cell death different from apoptosis, which supports cell survival and metabolism by degrading abnormal proteins or organelles within the cell to produce energy, which is an important mechanism for the degradation and recycling of intracellular components. In recent years, plenty of studies have found that autophagy participates in the occurrence and development of EMs. Previous studies reported that the level of autophagy in ectopic lesions of patients with EMs is lower than that in endometrial tissue of normal patients, and that the cyclical changes of autophagy in ectopic endometrial tissue of patients with EMs disappear. However, there are still a small number of studies demonstrate the higher levels of autophagy in ectopic lesions in patients with EMs. The complex environment of EMs ectopic lesion includes many factors that affect the level of autophagy, such as estrogen and progestin, hypoxia and oxidative stress, pathogen infection and iron overload, etc. In addition, autophagy plays a dual role in the occurrence development of EMs, it can not only hinder the progression of EMs by inhibiting the inflammatory response, promoting the immune system′s ability to clear lesions and inhibiting the fibrosis of the lesions, but also promote the progression of EMs by promoting the survival, migration and invasion of ectopic endometrial stromal cells.

Key words: Autophagy, Endometriosis, Autophagy-related proteins, Beclin-1 protein, Therapy