br Acknowledgements Authors wish to thank Sabanci

Acknowledgements Authors wish to thank Sabanci University (Turkey), Tubitak (Cost Eu-Ros, 113Z463), and the University of Turin (Italy) for supporting this work. Beyza Vurusaner is supported by Sabanci University Post-doctoral research scholarship.
Introduction Endometriosis is defined as the presence of functional uterine glands and stroma outside the uterine cavity including ovaries and pelvic peritoneum, rectovaginal septum. Endometriosis is an estrogen-dependent disorder of the women reproductive tract and the third leading cause of gynecologic hospitalization in the USA [1], [2]. It is indicated that endometriosis is one of the most common causes of chronic pelvic pain, infertility, dysmenorrhea, dyspareunia, dysuria and dyschezia, and affects an estimated 10% of the female population of reproductive age and 20–50% of infertile women [3], [4], [5]. There are several theories have been proposed underlying the pathogenesis of endometriosis. Among the various views, Sampson's theory of retrograde menstruation is the most widely accepted because it was observed that retrograde menstruation occurs in up to 90% of all women [6], [7]. Sampson's theory described that the menstrual debris travels not only anterogradely to the vagina, but also through the fallopian tube into the peritoneal cavity in a retrograde manner and implants in the dependent areas of peritoneum during menstruation [6], [7]. Actually, as studies continued, it was acceptable that the pathogenesis of endometriosis is polyfactorial which involved in reflux menstruation, hormonally mediated proliferation and apoptosis [8], [9], [10], hematologic spread, inflammation, immune response and genetic factors [2]. Autophagy is a pathway by which cytoplasmic components, including intracellular soluble macromolecules, organelles and microorganisms, is delivered to Microcystin-LR for degradation [11]. Studies supported that autophagy exists at basal level in all cell types. However, defects in autophagy underlie the pathogenesis of many diseases. It is worth mentioning in advance that autophagy is proved to act as a double-edged sword in multiple diseases which depend on different context [12]. In these years, accumulating researches present potential evidence that the progression of endometriosis was crucially implicated in autophagy, and seemingly opposing concepts concerning the role of autophagy in endometriosis have been proposed, with evidence that autophagy was up or down-regulated in endometriosis [5], [13]. So autophagy in endometriosis: friend or foe? In this mini review, we aim to explore and summarize the latent mechanism of autophagy in endometriosis from the recent studies and discuss which may contribute to the abnormal level of autophagy in endometriosis.
Conclusion and perspectives From all these studies, it is clear that there is an intimate relationship between autophagy and endomtriosis (Fig. 1). But autophagy in endometriosis: friend or foe? One the one hand, researches observe a down-regulation of autophagy in endometriosis. The related mechanism is implicated in the inhibition of mTOR by PI3K/AKT signaling pathway. Furthermore, the suppression of autophagy by CXCL12-dependent NF-κB pathway also contributes to endometriosis. In addition, the drugs use for endometriosis treatment is involved in the enhancing of autophagy. One the other hand, up-regulation of autophagy in endometriosis also is observed by studies. Hypoxia, decreased susceptibility to p53 and high expression of OH-1 contribute to the autophagy up-regulation. Besides, angiogenesis, ions channel, and iron may exert functions in autophagy in endometriosis. It is worthy mentioned that autophagy seems unchanged during menstrual cycle in endometriosis. Nevertheless, autophagy is a friend or foe in endometriosis is puzzling. In view of the results of these studies included only a handful of samples, further studies are required to investigate the exact role of autophagy in endometriosis, especially the in vivo studies and more autophagy-related protein should be detected. Moreover, using autophagy inhibitor will be contributed to confirm the exact role of autophagy in endometriosis.