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The proteins Heart of Glass (HEG1) and Rasip1 are both essential for cardiovascular development; and directly bind to each other to guide Rasip1 to endothelial cell junctions to support vascular integrity.

Vascular endothelial cells in the brain, heart and lung exhibit tissue-specific heterogeneity and plasticity, expressing genes that were traditionally thought to be only expressed by the surrounding parenchymal tissue cells.

EphrinB2/EphB4-mediated regulation of cytoskeletal contractility is a key homeostatic mechanism of lymphatic endothelial cell-cell junction maintenance, and provides a potential target for therapeutic modulation of lymphatic vessel permeability and function.

Organ and vessel-type-specific differences in endothelial cell barrier composition and properties uncover the distinct importance of the major tight junction protein Claudin5 in restricting agonist-induced leakage.

Comprehensive proteomic investigation and functional studies unravel an essential role of differentiated glioma cell-secreted fibromodulin (FMOD) in regulating glioblastoma tumor growth by inducing angiogenesis by activating integrin-dependent Notch signaling in endothelial cells, highlighting FMOD as a potential therapeutic target.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.

Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Caffeine modulates the genetic risk for cardiovascular disease through changes in target gene expression, likely due to regulation of transcription factor binding.

Several previously proposed cell-surface receptors for hantaviruses could be deleted in endothelial cells with little or no effect on infection, indicating that critical hantavirus entry factors remain undiscovered.

Apelin signaling promotes sprouting behavior of endothelial cells by modulating their metabolic state.