Abstract
Endothelial-mesenchymal transition (EndMT) is a biological process in which endothelial cells lose intercellular junctions and endothelial characteristics under specific pathophysiological stimuli and acquire mesenchymal traits. It plays a critical role in cardiac development, tissue fibrosis, tumor metastasis, atherosclerosis, and other diseases. In recent years, growing evidence has demonstrated that epigenetic modifications and post-translational modifications are central to the precise regulation of EndMT initiation and progression. This review systematically elaborates on how epigenetic mechanisms-such as DNA methylation, histone modifications, and non-coding RNAs-as well as post-translational modifications, including protein phosphorylation, acetylation, and ubiquitination, regulate EndMT by modulating key signaling pathways (e.g., TGF-β, Wnt, Notch) and transcription factors (e.g., Snail, Slug, Twist, ZEB1/2). A deeper understanding of these regulatory networks may provide novel diagnostic biomarkers and therapeutic strategies for diseases targeting EndMT.