A mechanisms of endometrial fibrosis and the potential application of stem cell therapy.

Fibrosis diseases result from excessive accumulation of extracellular matrix proteins which lead to normal tissue being replaced by fibrotic tissue or scar and eventually cause organ failure. Endometrial fibrosis is defined as the physiological endometrium becoming librosed, also known as intrauterine adhesions (IUA) or Asherman's syndrome, which progressively impairs endometrial function. On the basis of the fibrosis pathology, prevention of endometrial fibrosis is fundamental for IUA treatment, and elucidating the cellular and molecular mechanisms underlying endometrial fibrosis is imperative. Myofibroblasts play a crucial role in fibrosis formation. Thus, understanding the myofibroblasts' proliferation and the key signaling pathways is essential for implementing novel therapies of fibrosis diseases. Stem cell therapy is an emerging and potentially powerful therapeutic modality for refractory severe IUA patients in recent years. In this review, we discuss the role of myofibroblasts, summarize the key cellular and molecular mechanisms participating in the endometrial fibrosis process, and attempt to explain the anti-fibrosis mechanism under stem cell therapy.