Abstract

This editorial refers to ‘Endothelial Jag1-RBPJ signalling promotes inflammatory leucocyte recruitment and atherosclerosis’ by M. Nus et al. , pp. 568–580 Notch signalling is an evolutionary conserved regulator of vascular and immune cell development and homeostasis.1,2 In this issue of Cardiovascular Research , Nus et al. 3 now report a new role of endothelial Notch signalling in regulating vascular homeostasis by regulating vascular inflammation in atherosclerosis. Activation of Notch receptors is controlled by membrane-bound Notch ligands consisting of the Jagged (Jag) and Delta-like (Dll) gene families.2 Notch signalling regulates endothelial cell proliferation, migration, and sprouting angiogenesis and thereby critically regulates vascular morphogenesis and function.1,4,5 In response to ischaemic vascular injury, Notch activation mediates vascular repair and regeneration, which ensures neovascularization of tissues, organs, and recovery of their function.6,7 In this issue of Cardiovascular Research , Nus et al. 3 now report that endothelial Notch signalling regulates homing of leucocytes to the vascular wall during atherosclerosis. They demonstrate that the Notch ligand Jag1 and Notch signalling are upregulated in atherosclerotic human and mouse arteries. Furthermore, …

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