Endothelial cells (ECs), which form the monolayer lining the vasculature, serve as critical gatekeepers of vascular homeostasis. They actively coordinate immune cell recruitment, adhesion, migration, and activation. Through tightly controlled expression and secretion of chemokines, cytokines, adhesion molecules, and immunomodulatory proteins, ECs locally orchestrate immune responses. In atherosclerosis, ECs contribute to plaque formation, plaque instability, and local inflammation by facilitating immune cell activation and transmigration into the plaque. However, ECs are highly heterogeneous, with their phenotype and function influenced by vascular localization and disease stage. EC subpopulations are transcriptionally distinct and adopt to either proinflammatory or angiogenic phenotypes and differentially participate in immune modulation. This review discusses recent insights into the immunomodulatory functions of ECs in atherosclerosis and underscores the importance of EC heterogeneity in understanding endothelial-immune cell interactions.
Kesteren et al. (Sun,) studied this question.