Novel and common angiogenic mechanisms crucial for fenestrated brain capillary formation have been identified.

Both VEGF-C and VEGF-D can be activated by KLK3/PSA and Cathepsin D, producing two novel VEGF-C forms and the known VEGFR-2-specific form of VEGF-D.

Identification of a developmental mechanism critical for the generation of brain vessel heterogeneity.

Visualization and quantitative analyses of calcium ion oscillations in the endothelial cells of zebrafish embryos reveal how vascular endothelial growth factor (VEGF) and Dll4/Notch signaling regulate sprouting angiogenesis.

Bulk and single-cell RNA-seq data demonstrated that muscle stem cells express low levels of canonical endothelial cell markers, including VEGFA receptors, and VEGFA-FLT1 pathway has a drastic effect on muscle stem cell survival through AKT1 in vitro and in vivo.

Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Elabela-Apelin receptor signaling is a novel pathway that regulates angioblast migration, instead of the proposed migration regulation through Vascular endothelial growth factor.

Compositional changes alter actin binding by phase separated T cell signaling clusters, enabling cluster movement by distinct actin networks.

In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.

Primary cilia on endothelial cells are required for VEGF-A/ VEGFR2-dependent signaling, islet vascularization and, consequently, nutrient delivery and insulin disposal.