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.
Vascular leakage from pathological vessels in retinopathy aggravates the disease, but endothelial junction stability and barrier integrity can be restored by blocking formation of nitric oxide.
Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.
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.
Genome-wide integration of transcriptome, accessible chromatin, and DNA methylome data from vascular endothelial cells lays the foundation for understanding the gene regulatory circuits that generate organ-specific vascular specialization.
The eye produces a protein that inhibits the growth of blood vessels in the deep retina, which includes the photoreceptor layer, and disruption of this process can lead to blindness.
Tissue-specific temporal regulators impinge on the VEGF/Delta-Notch pathway to vary tip cell selection pace yielding diverse densities of vascular network.
Endothelial YAP/TAZ shape the developing vasculature by orchestrating mechanical inputs with BMP signalling to promote junctional VE-Cadherin turnover and cellular rearrangements.
Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.
