Role of protein post-translational modifications in unexplained recurrent pregnancy loss.

Abstract

Unexplained recurrent pregnancy loss (URPL) is a complex pathological condition that poses significant challenges for women of childbearing age. As a critical component of epigenetics, post-translational modifications (PTMs) not only regulate protein expression and enhance its diversity but also modulate interactions between proteins and other molecules. PTMs play an essential role in the onset and progression of URPL. For example, methylation modifications can hinder decidualization and regulate trophoblast migration and invasion. Phosphorylation modifications can balance regulatory T cells (Treg)/T helper 17 cells (Th17), polarize macrophages, alter dendritic cell populations, and promote trophoblast apoptosis. Acetylation modifications can induce trophoblasts autophagy and suppress M2 macrophage polarization. Ubiquitination modifications can modulate trophoblast migration and invasion and disrupt the immune microenvironment. Glycosylation modifications can inhibit trophoblast migration and invasion, while lactylation modifications maintain endometrial receptivity. The role of PTMs in URPL highlights their potential as a research entry point and therapeutic target for this condition.