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.
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.
Identification of the R(+)-propranolol enantiomer as an inhibitor of the SOX18 transcription factor activity breaks open potential of drug repurposing in vascular diseases.
