Key result
Excessive NO production and nitrosative stress linked to ER stress in oxLDL-induced endothelial dysfunction.
Why the study?
The precise molecular mechanisms by which oxLDL and oxysterols induce endoplasmic reticulum stress, inflammation, and apoptosis in endothelial dysfunction remain incompletely understood.
This review provides a conceptual framework linking nitrosative stress to endoplasmic reticulum stress in endothelial dysfunction, identifying potential novel therapeutic targets.
May implicate nitrosative-ER stress interplay in oxLDL endothelial dysfunction; leaves open mechanistic validation and therapeutic targeting.
Oxidized LDL (oxLDL) and oxysterols are known to play a crucial role in endothelial dysfunction (ED) by inducing endoplasmic reticulum stress (ERS), inflammation, and apoptosis. However, the precise molecular mechanisms underlying these pathophysiological processes remain incompletely understood. Emerging evidence strongly implicates excessive nitric oxide (NO) production in the progression of various pathological conditions. The accumulation of reactive nitrogen species (RNS) leading to nitrosative stress (NSS) and aberrant protein S-nitrosylation contribute to NO toxicity. Studies have highlighted the involvement of NSS and S-nitrosylation in perturbing ER signaling through the modification of ER sensors and resident isomerases in neurons. This review focuses on the existing evidence that strongly associates NO with ERS and the possible implications in the context of ED induced by oxLDL and oxysterols. The potential effects of perturbed NO synthesis on signaling effectors linking NSS with ERS in endothelial cells are discussed to provide a conceptual framework for further investigations and the development of novel therapeutic strategies targeting ED.
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Nasoni et al. (2023) conducted a review in Endothelial dysfunction. Nitrosative stress and aberrant protein S-nitrosylation was evaluated. This review highlights the association between excessive nitric oxide production, nitrosative stress, and endoplasmic reticulum stress in the context of oxLDL/oxysterol-induced endothelial dysfunction.
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