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processes are essential in vascular remodelling where structural changes to the blood vessel wall are necessary during normal physiology, aging, injury, and disease. Cells act in response to the ECM and remodel, but this process becomes impaired in vascular

existing vessel in two. This process is achieved by insertion of a cellular pillar into a vascular lumen. It was first described in neonatal rats and, although it occurs in regions of the vascular network with minimal hemodynamic forces, it seems that is

patency of their normal counterparts. Tumour blood vessel normalisation restores vascular function thereby increasing tumour perfusion and alleviating hypoxia. This in turn increases the response to therapy, suppresses endothelial-to-mesenchymal transition

first to develop during mammalian embryogenesis. While the primitive vascular plexus arises de novo from mesoderm-derived cells (the so-called angioblasts), the majority of vessels develop by sprouting angiogenesis, a process of vessel formation from

similarities and differences in calcific pathological development between heart valves and blood vessels. Of particular focus is the role that oscillatory blood flow patterns play in biomechanical-induced activation of diseased pathways in valvular vs vascular

the primitive vascular plexus and the heart during embryonic development, via the differentiation of endothelial cell precursors (hemangioblasts) into endothelial cells ( 4 ). Angiogenesis refers to the formation of new vessels from pre-existing ones

results in splitting of the primary vessel into two new ones. Vessel splitting may occur in the virtual absence of endothelial proliferation and can allow rapid expansion of a vascular network, which, in contrast to sprouting angiogenesis, does not require

vessels, four Cxs have been found in ECs and SMCs, specifically Cx37, Cx40, Cx43 and Cx45. The size and abundance of GJs as well as the expression patterns of individual Cxs has been shown to vary in different regions of the vascular tree and with the

of VEGF as a therapeutic tool, however, has proven to be tricky, as long-term VEGF administration promotes vascular permeability and immature angiogenesis forming non-functional vessels. The same holds true for VEGF-C, whereas overexpression of VEGF

environment ( 5 ). Other comprehensive reviews discussed the differentiation of MSCs to tissue-specific cells under different conditions ( 6 , 7 ). In this review, we aim to provide an overview on the contribution of large-vessel resident MSCs to vascular