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Ageing‐induced internalization and degradation of VE‐cadherin leads to vascular dysfunction

Ageing‐induced internalization and degradation of VE‐cadherin leads to vascular dysfunction With increasing age, the arterial system undergoes deterioration which contributes to cardiovascular disease, a leading cause of morbidity and mortality worldwide. Age‐dependent deterioration of the vascular network is partly mediated by endothelial cell dysfunction, which is characterized by reduced nitric oxide (NO) levels, impaired endothelial cell barrier, increased susceptibility to apoptosis, and an overall pro‐inflammatory phenotype. The protective role of endothelial cells in the vasculature is thought to be mediated by increased clustering of VE‐cadherins at the adherens junctions, which promotes protective signalling by amplifying endothelial NO‐mediated dilatation and increasing vascular stability. VE‐cadherins are calcium‐dependent glycoproteins that play a vital role in proper endothelial cell‐to‐cell contact and allow transfer of intracellular signals from one cell to another. It has been suggested that they may play a protective role under pathological conditions, but their role in ageing‐induced vascular disease has not been thoroughly investigated.In a recent issue of The Journal of Physiology, Chang et al. () investigated the association between ageing and vascular dysfunction of the arterial system. The authors aimed to determine the contribution of altered endothelial adherens junctions in vascular disease. They provided direct evidence of ageing‐induced molecular changes that promote endothelial dysfunction through VE‐cadherin internalization and degradation. Specifically, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Ageing‐induced internalization and degradation of VE‐cadherin leads to vascular dysfunction

Shah, Haisam; Brar, Karmen
The Journal of Physiology , Volume 596 (2) – Jan 15, 2018
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References (5)

Publisher
Wiley
Copyright
Journal compilation © 2018 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/JP275495
Publisher site
See Article on Publisher Site

Abstract

With increasing age, the arterial system undergoes deterioration which contributes to cardiovascular disease, a leading cause of morbidity and mortality worldwide. Age‐dependent deterioration of the vascular network is partly mediated by endothelial cell dysfunction, which is characterized by reduced nitric oxide (NO) levels, impaired endothelial cell barrier, increased susceptibility to apoptosis, and an overall pro‐inflammatory phenotype. The protective role of endothelial cells in the vasculature is thought to be mediated by increased clustering of VE‐cadherins at the adherens junctions, which promotes protective signalling by amplifying endothelial NO‐mediated dilatation and increasing vascular stability. VE‐cadherins are calcium‐dependent glycoproteins that play a vital role in proper endothelial cell‐to‐cell contact and allow transfer of intracellular signals from one cell to another. It has been suggested that they may play a protective role under pathological conditions, but their role in ageing‐induced vascular disease has not been thoroughly investigated.In a recent issue of The Journal of Physiology, Chang et al. () investigated the association between ageing and vascular dysfunction of the arterial system. The authors aimed to determine the contribution of altered endothelial adherens junctions in vascular disease. They provided direct evidence of ageing‐induced molecular changes that promote endothelial dysfunction through VE‐cadherin internalization and degradation. Specifically,

Journal

The Journal of Physiology – Wiley

Published: Jan 15, 2018

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