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.

Single-cell RNA sequencing reveals extensive endothelial cell (EC) heterogeneity throughout the lung vasculature and identifies two distinct populations, Car4-high ECs and proliferative ECs, that preferentially respond to lung injury.

Activation of Wnt/β-catenin signaling in endothelial progenitors derived from human pluripotent stem cells partially induces the specialized blood–brain barrier phenotype while the same treatment in matured endothelial cells is less efficacious.

A rare population of endothelial cells emerges from a bipotent muscle progenitor population in the paraxial mesoderm and provides niche support to induce hematopoietic stem cells.

Adenoviral CRISPR/Cas9 gene knockdown of mutant Col8a2 achieves structural and functional rescue of murine Fuchs’ endothelial corneal dystrophy, the first demonstration of post-mitotic CRISPR-based knockdown for phenotypic restoration.

Endothelial dysfunction due to cardiovascular disease risk factors explained by cardiac endothelial cell transcriptome remodelling.

Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.

The acquisition of vascular quiescence during transition to adulthood is driven by distinct transcriptional and epigenetic programs of pro- and anti-angiogenic genes, with the most prominent effect on the suppression of TGFß family signaling.

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

METTL3 and m6A modifications could alleviate endothelial activation and atherogenesis through accelerated degradation of oscillatory flow-induced EGFR mRNA expression.