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Updated: Mar 18, 2026
06:35
Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
18.9K
Role of endoplasmic reticulum stress in endothelial dysfunction
A Cimellaro1, M Perticone2, T V Fiorentino1
1Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, Viale Europa, Catanzaro, 88100, Italy.
Summary
Endoplasmic reticulum (ER) stress contributes to endothelial dysfunction (ED) and cardiovascular disease (CVD). Targeting ER stress may offer a novel therapeutic strategy to prevent vascular damage and slow the progression of cardiovascular events.
Area of Science:
- Cardiovascular Science
- Cellular Biology
- Pathophysiology
Background:
- Endoplasmic reticulum (ER) stress is linked to cardiovascular disease (CVD) pathogenesis.
- Endothelial dysfunction (ED) is a primary factor in CVD development.
- ER stress is a significant contributor to vascular damage caused by metabolic risk factors.
Purpose of the Study:
- To review experimental findings on ER stress-related endothelial dysfunction.
- To elucidate the mechanisms linking ER stress and ED.
- To highlight the role of ER stress in cardiovascular pathology.
Main Methods:
- Review of experimental studies on ER stress and ED.
- Analysis of mechanisms underlying ER stress-induced vascular damage.
- Examination of evidence from animal models and human endothelial cells.
Main Results:
- Various risk factors (hyperhomocysteinemia, hyperlipidemia, hyperglycemia, inflammation) induce ED via amplified ER stress.
- ER stress mediates vascular damage, exacerbating inflammation and oxidative stress.
- An unchecked ER stress response is central to ED and CVD pathogenesis.
Conclusions:
- ER stress is a key mediator in the development of endothelial dysfunction and cardiovascular disease.
- Therapeutic strategies targeting ER stress may prevent vascular damage.
- Counteracting ER stress could slow the progression from ED to cardiovascular events.
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