Optogenetic activation of Rho GTPases provides spatiotemporal control over endothelial cell shape and enables control over endothelial barrier function by manipulating the cell-cell overlap with blue light.

Intravascular triglyceride hydrolysis by lipoprotein lipase is crucial for delivering lipid nutrients to vital tissues, such as the heart, skeletal muscle, and adipose tissue.

LIPG, a lipoprotein lipase, executes its oncogenic function in human basal-like triple-negative breast cancer through its functional involvement in DTX3L-ISG15 signaling, an interferon-related pathway that regulates protein functionality by ISGylation.

Building on previous work (Mysling et al., 2016), it is shown that angiopoietin-like protein 4 (ANGPTL4) inhibits lipoprotein lipase activity by catalyzing the unfolding of its hydrolase domain.

The cAMP-dependent protein kinase A controls the switch from actively sprouting new blood vessel formation to vessel quiescence by reducing endothelial autophagy through phosphorylation-mediated destabilisation of ATG16L1.

Brain natriuretic peptide supplementation can increase cardiac neovascularization in infarcted hearts by stimulating endogenous endothelial cell proliferation and proliferation of precursor cells, which will differentiate into endothelial cells.

A V-ATPase component and protein kinase D are required for the segregation of Weibel–Palade bodies from the trans-Golgi network.

The expression of the lipoprotein lipase (LPL) transporter GPIHBP1 in glioma capillaries promotes the LPL-mediated processing of triglyceride-rich lipoproteins, thereby providing lipid nutrients for glioma cells.

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.

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