Abstract: Endothelial-to-Mesenchymal Transition (EndMT) is a regulatory mechanism integral to the normal developmental processes of the organism, playing a pivotal role in sustaining the homeostasis of the intravascular milieu. However, when the internal environment exceeds the endothelium's compensatory capacity, excessive EndMT can precipitate pathological alterations. EndMT is particularly significant in the pathogenesis of pulmonary diseases, including pulmonary fibrosis, pulmonary hypertension, and lung cancer. The regulatory mechanisms underlying EndMT are intricate and multifaceted. Numerous signaling pathways have been implicated in EndMT modulation, with the TGF-β pathway emerging as a central inducer. Furthermore, research has identified that epigenetic modifications, metabolic processes, hypoxia, inflammatory cytokines, and oxidative stress all contribute to the regulation of EndMT. This complexity renders the interplay between EndMT and pulmonary vascular diseases exceedingly intricate. In this manuscript, we provide a comprehensive overview of the signaling pathways and other influencing factors that govern EndMT. Concurrently, we meticulously delineate potential therapeutic targets to offer novel avenues and insights for the management of pulmonary diseases. Our synthesis of the current understanding of EndMT regulation is intended to inform future research and clinical strategies, potentially leading to more effective interventions for patients afflicted with pulmonary disorders.
Huang et al. (Wed,) studied this question.