Cardiology, blood circulation, phlebology, Cardiologie, appareil circulatoire, phlébologie, Sciences biologiques et medicales, Biological and medical sciences, Sciences medicales, Medical sciences, Pharmacologie. Traitements medicamenteux, Pharmacology. Drug treatments, Toxicité des médicaments et traitement des toxicités dues aux médicaments, Drug toxicity and drugs side effects treatment, Toxicité: sang, Toxicity: blood, Cardiologie. Appareil circulatoire, Cardiology. Vascular system, Vaisseaux sanguins et lymphatiques, Blood and lymphatic vessels, Athérosclérose (généralités, étude expérimentale), Atherosclerosis (general aspects, experimental research), Maladies vasculaires des membres. Pathologie de la veine cave. Maladies vasculaires diverses, Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous, Pathologie des vaisseaux sanguins, Vascular disease, Vaso sanguíneo patología, Apoptose, Apoptosis, Athérosclérose, Atherosclerosis, Ateroesclerosis, Macrophage, Macrófago, Pathologie de l'appareil circulatoire, Cardiovascular disease, Aparato circulatorio patología, Stress, Estrés, ER stress, apoptosis, atherosclerosis, macrophages, and unfolded protein response
Endoplasmic reticulum (ER) stress is triggered by perturbations in ER function such as those caused by protein misfolding or by increases in protein secretion. Eukaryotic cells respond to ER stress by activating 3 ER-resident proteins, activating transcription factor-6, inositol requiring protein-1, and protein kinase RNA-like ER kinase (PERK). These proteins direct signaling pathways that relieve ER stress in a process known as the unfolded protein response (UPR). In pathological settings, however, prolonged UPR activation can promote cell death, and this process has recently emerged as an important concept in atherosclerosis. We review here the evidence for UPR activation and cell death in macrophages, smooth muscle cells, and endothelial cells in the context of advanced atherosclerosis as well as the existing literature regarding mechanisms of UPR-induced cell death. Knowledge in this area may suggest new therapeutic targets relevant to the formation of clinically dangerous atherosclerotic plaques.