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Mechanisms of ER Stress-Induced Apoptosis in Atherosclerosis

Open access
Scull, Christopher M., Tabas, Ira·2011·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

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.

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Metadata

Authors
Scull, C. M., & Tabas, I.
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2011-12
Volume
31
Issue
12
Pages
2792-2797
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W2153139917
Cited by
197
References
2
FWCI
6.67
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Mechanisms of ER Stress-Induced Apoptosis in Atherosclerosis. https://app.cochat.ai/papers/10.1161/atvbaha.111.224881
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Scull, C. M., & Tabas, I. (2011). Mechanisms of ER Stress-Induced Apoptosis in Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/atvbaha.111.224881

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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