Aspirin inhibits endometrial fibrosis by suppressing theTGF‑β1‑Smad2/Smad3 pathway in intrauterine adhesions.

Abstract

Intrauterine adhesions (IUAs) represent one of the most common diseases in women of reproductive age. Patients with moderate-to-severe IUA can experience a decrease in normal menstrual patterns, amenorrhea and even infertility. At present, the first-line treatment strategies for IUAs in the clinical practice are hysteroscopic transuterine resection of adhesion and postoperative adjuvant therapy, including oestrogen. However, a high recurrence rate of IUAs remains. In recent years, studies have demonstrated that aspirin combined with oestrogen may significantly prevent the postoperative disease recurrence rate, improve endometrial receptivity and improve the conception rate by increasing endometrial blood supply and angiogenesis more effectively. The TGF-β1-Smad2/Smad3 pathway is one of the important mechanisms involved in endometrial fibrosis. However, whether aspirin can inhibit endometrial fibrosis through the TGF-β1-Smad2/Smad3 pathway to prevent postoperative re-adhesion remains to be elucidated. The results of the present study suggested that aspirin inhibits endometrial fibrosis by suppressing the TGF-β1-Smad2/Smad3 pathway, which may provide new hypotheses for the mechanism of action of aspirin in the treatment of IUAs.