ArticleBiochimica et biophysica acta2014
Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 144 citations in OpenAlex.
- Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load.Clinical science (London, England : 1979) · 2016Trial
- Mitigating sepsis-induced vascular endothelial dysfunction through Niban phosphorylation.Vascular medicine (London, England) · 2026Article
- Review
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Novel insights into beta cell ER stress CHOP and its role in HFpEF development.Cardiovascular diabetology · 2025Article
- Endothelial CHOP as a central mechanism in renovascular hypertension-induced vascular endothelial dysfunction and cardiac fibrosis.Cellular and molecular life sciences : CMLS · 2025Article
- Celastrol improves endothelial function in diet-induced obesity mice via attenuating endoplasmic reticulum stress through the activation of AMPK pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Identification of endoplasmic reticulum stress-associated lncRNAs influencing inflammation and VSMC function in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2025Article
- Endoplasmic reticulum stress is attenuated by glycolysis in lymphatic malformations.Pediatric research · 2024Article
- Endoplasmic Reticulum Stress Induces Vasodilation in Liver Vessels That Is Not Mediated by Unfolded Protein Response.International journal of molecular sciences · 2024Article
- Pridopidine subtly ameliorates motor skills in a mouse model for vanishing white matter.Life science alliance · 2024Article
- Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts by inhibiting CHOP-mediated NF-κB expression.Frontiers in pharmacology · 2024Article
- Article
- Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023Review
- Interleukin-1β Disruption Protects Male Mice From Heart Failure With Preserved Ejection Fraction Pathogenesis.Journal of the American Heart Association · 2023Article
- Aging reduces calreticulin expression and alters spontaneous calcium signals in astrocytic endfeet of the mouse dorsolateral striatum.npj aging · 2023Article
- Article
- Chitooligosaccharide prevents vascular endothelial cell apoptosis by attenuation of endoplasmic reticulum stress via suppression of oxidative stress through Nrf2-SOD1 up-regulation.Pharmaceutical biology · 2022Article
- Shrimp Lipid Prevents Endoplasmic Reticulum-Mediated Endothelial Cell Damage.Foods (Basel, Switzerland) · 2022Article
- Down-regulation of AMPK/PPARδ signalling promotes endoplasmic reticulum stress-induced endothelial dysfunction in adult rat offspring exposed to maternal diabetes.Cardiovascular research · 2022Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
backgroundWe recently reported that ER stress plays a key role in vascular endothelial dysfunction during hypertension. In this study we aimed to elucidate the mechanisms by which ER stress induction and oxidative stress impair vascular endothelial function. METHODOLOGY/PRINCIPAL
findingsWe conducted in vitro studies with primary endothelial cells from coronary arteries stimulated with tunicamycin, 1μg/mL, in the presence or absence of two ER stress inhibitors: tauroursodeoxycholic acid (Tudca), 500μg/mL, and 4-phenylbutyric acid (PBA), 5mM. ER stress induction was assessed by enhanced phosphorylation of PERK and eIF2α, and increased expression of CHOP, ATF6 and Grp78/Bip. The ER stress induction increased p38 MAPK phosphorylation, Nox2/4 mRNA levels and NADPH oxidase activity, and decreased eNOS promoter activity, eNOS expression and phosphorylation, and nitrite levels. Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. To study the effects of ER stress induction in vivo, we used C57BL/6J mice and p47phox(-/-) mice injected with tunicamycin or saline. The ER stress induction in mice significantly impaired vascular endothelium-dependent and independent relaxation in C57BL/6J mice compared with p47phox(-/-) mice indicating NADPH oxidase activity as an intermediate for ER stress in vascular endothelial dysfunction. CONCLUSION/SIGNIFICANCE: We conclude that chemically induced ER stress leads to a downstream enhancement of p38 MAPK and oxidative stress causing vascular endothelial dysfunction. Our results indicate that inhibition of ER stress could be a novel therapeutic strategy to attenuate vascular dysfunction during cardiovascular diseases.
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