Cardiovascular disease continues to be the leading cause of death in industrialised societies.
The idea that the arterial smooth muscle cell (ASMC) plays a key role in regulating many vascular
pathologies has been gaining importance, as has the realisation that not enough is known about
the pathological cellular mechanisms regulating ASMC function in vascular remodelling. In the past
decade endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have been recognised
as a stress response underlying many physiological and pathological processes in various
vascular cell types. Here we summarise what is known about how ER stress signalling regulates phenotypic
switching, trans/dedifferentiation and apoptosis of ASMCs and contributes to atherosclerosis,
hypertension, aneurysms and vascular calcification.