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Updated: Jul 20, 2025
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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
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When nitrosative stress hits the endoplasmic reticulum: Possible implications in oxLDL/oxysterols-induced endothelial
M G Nasoni1, R Crinelli1, L Iuliano2
1Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Free Radical Biology & Medicine
|August 6, 2023
Summary
Oxidized LDL and oxysterols contribute to endothelial dysfunction via endoplasmic reticulum stress. This review explores how nitric oxide overproduction and nitrosative stress link to this stress, impacting endothelial cells.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Molecular Medicine
Background:
- Oxidized low-density lipoprotein (oxLDL) and oxysterols are key contributors to endothelial dysfunction (ED).
- Endoplasmic reticulum stress (ERS), inflammation, and apoptosis are induced by oxLDL and oxysterols, but mechanisms are unclear.
- Excessive nitric oxide (NO) production, reactive nitrogen species (RNS), nitrosative stress (NSS), and protein S-nitrosylation are implicated in pathology.
Purpose of the Study:
- To review the association between NO and ERS in oxLDL/oxysterol-induced ED.
- To elucidate the molecular mechanisms linking NSS and ERS in endothelial cells.
- To propose a framework for therapeutic strategies targeting ED.
Main Methods:
- Literature review of existing evidence.
- Analysis of molecular pathways involving NO, RNS, NSS, and ERS.
- Focus on endothelial cell signaling.
Main Results:
- Evidence links NO overproduction and NSS to ERS.
- NSS and S-nitrosylation can perturb ER signaling pathways.
- Perturbed NO synthesis may affect signaling effectors in endothelial cells.
Conclusions:
- Nitric oxide plays a significant role in ERS within the context of oxLDL/oxysterol-induced ED.
- Understanding the interplay between NSS and ERS is crucial for ED.
- Further research can guide novel therapeutic interventions for ED.
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