Journal
REDOX BIOLOGY
Volume 57, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.redox.2022.102473
Keywords
Atherosclerosis; Carotid artery stenosis; NADPH oxidase 4; Plaques
Categories
Funding
- European Stroke Research Foundation (ESRF)
- Carl Gustav Carus Promotionskolleg?
- Medical Faculty of the TU Dresden
- Cardio-Pulmonary Institute (CPI) [IRTG 2251]
- Deutsche Forschungsgemeinschaft (DFG) [MO 1695/4-1 and 5-1]
- German Centre for Cardiovascular Research (DZHK)
- [390649896]
- [47081312]
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The study found that low NOX4 mRNA expression is associated with an increased risk for symptomatic carotid artery stenosis and reduced plaque stabilizing mechanisms, suggesting protective effects of NOX4 in human advanced atherosclerosis.
Carotid artery stenosis (CAS) develops from atherosclerotic lesions and plaques. Plaque rupture or stenosis may result in occlusion of the carotid artery. Accordingly, the asymptomatic disease becomes symptomatic, charac-terized by ischemic stroke or transient ischemic attacks, indicating an urgent need for better understanding of the underlying molecular mechanisms and eventually prevent symptomatic CAS. NOX4, a member of the NADPH oxidase family, has anti-atherosclerotic and anti-inflammatory properties in animal models of early athero-sclerosis. We hypothesized that NOX4 mRNA expression is linked to protective mechanisms in CAS patients with advanced atherosclerotic lesions as well. Indeed, NOX4 mRNA expression is lower in patients with symptomatic CAS. A low NOX4 mRNA expression is associated with an increased risk of the development of clinical symptoms. In fact, NOX4 appears to be linked to plaque stability, apoptosis and plaque hemorrhage. This is supported by cleaved caspase-3 and glycophorin C and correlates inversely with plaque NOX4 mRNA expression. Even healing of a ruptured plaque appears to be connected to NOX4, as NOX4 mRNA expression correlates to fibrous cap collagen and is reciprocally related to MMP9 activity. In conclusion, low intra-plaque NOX4 mRNA expression is associated with an increased risk for symptomatic outcome and with reduced plaque stabilizing mechanisms suggesting protective effects of NOX4 in human advanced atherosclerosis.
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