The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis
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Discussion
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Implication
Mechanistic review uncovers how chronic endoplasmic reticulum stress drives plaque necrosis in vascular cells, highlighting therapeutic targets for advanced atherosclerosis.
Key Points
- To examine the mechanistic role of chronic endoplasmic reticulum stress and the unfolded protein response in driving the progression of atherosclerotic lesions.
- Synthesized molecular and in vivo evidence evaluating unfolded protein response activation in arterial wall cells, focusing on advanced lesional macrophages and endothelial cells.
- Evaluated the impact of upstream cellular stressors, including oxidative stress, oxysterols, intracellular cholesterol, and metabolic conditions like obesity and diabetes.
- Prolonged endoplasmic reticulum stress triggers macrophage apoptosis, which promotes plaque necrosis when clearance of apoptotic cells is impaired.
- Sustained activation of the unfolded protein response stimulates pro-inflammatory signaling pathways in macrophages and induces endothelial cell death under atheroprone shear stress.
Cite This Study
Ira Tabas (2010) studied this question.