自噬在宫腔粘连发展机制中的研究进展OA

Intrauterine adhesion(IUA)is a fibrotic disease caused by endometrial injury,which seriously affects female fertility and reproductive health.The core pathological features of IUA are epithelial-mesenchymal transition(EMT)of the endometrium and excessive deposition of the extracellular mechanism(ECM),in which autophagy plays a key role.Studies have shown that the expression of autophagy markers in the endometrium of IUA patients is significantly reduced,and the impaired autophagy flux leads to the activation of EMT,abnormal accumulation of collagen,resulting in fibrosis of the endometrium.Autophagy affects processes such as fibrosis,inflammatory response and macrophage polarization by regulating multiple signaling pathways,including Sonic Hedgehog(SHH),type Ⅱ iodothyronine deiodinase-mitogen-activated protein kinase/extracellular signal-regulated kinase-mammalian target of rapamycin(DIO2-MAPK/ERK-MTOR),PTEN-induced kinase 1/Parkin(PINK1/Parkin).In addition,autophagy-related genes,the miRNA-mRNA regulatory network,and the extended competing endogenous RNA(ceRNA)regulatory network mechanism also play important roles in regulating IUA by autophagy.This article systematically reviews the regulatory role of autophagy in IUA,providing new ideas for improving the prognosis and reproductive outcomes of patients.