Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 94-105 |
| Number of pages | 12 |
| Journal | Current Cardiology Reviews |
| Volume | 13 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2017 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Atherosclerosis
- ER stress
- Vascular calcification
- Vascular smooth muscle cell
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