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Updated: Jan 22, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
NOX1 Negatively Modulates Fibulin-5 in Vascular Smooth Muscle Cells to Affect Aortic Dissection
Xiaoping Hu1, Wanli Jiang2, Zhiwei Wang1
1Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University.
Abstract:
Aortic dissection (AD) diseases are characterized by degeneration of the aortic media. Oxidative stress plays a crucial role in the development of AD. Reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (NOX1) deficiency reduces the incidence of aortic dissection induced by angiotensin II, but its mechanism remains to be further elucidated. The expression of Fibulin-5 is decreased in patients with AD, but its upstream mechanism is still unclear. This study was to clarify the relationship between NOX1 and Fibulin-5 in the AD. Results showed that the expressions of NOX1 and Fibulin-5 were increased and decreased in the AD, respectively. Next, by employing gain- and loss-of-function approaches in vitro, NOX1 negatively regulated Fibulin-5 in the vascular smooth muscle cells. Moreover, the blunted activity of NOX1 with VAS2870 could upregulate the expression of Fibulin-5. These findings indicate NOX1 is a negative modulator of Fibulin-5 in the AD.
Insights
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (NOX1) negatively regulates Fibulin-5 expression in aortic dissection (AD). This study clarifies NOX1
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Oxidative Stress Research
Background:
- Aortic dissection (AD) involves medial degeneration, with oxidative stress as a key factor.
- Reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (NOX1) shows protective effects in angiotensin II-induced AD, but its mechanism is unclear.
- Fibulin-5 expression is decreased in AD patients, and its upstream regulation requires elucidation.
Purpose of the Study:
- To investigate the relationship between NOX1 and Fibulin-5 in the context of aortic dissection (AD).
- To elucidate the regulatory mechanism of NOX1 on Fibulin-5 expression in vascular smooth muscle cells.
Main Methods:
- Analysis of NOX1 and Fibulin-5 expression levels in AD.
- In vitro gain- and loss-of-function studies in vascular smooth muscle cells.
- Pharmacological inhibition of NOX1 activity using VAS2870.
Main Results:
- NOX1 expression was increased, while Fibulin-5 expression was decreased in AD.
- NOX1 was found to negatively regulate Fibulin-5 expression in vascular smooth muscle cells.
- Inhibition of NOX1 activity with VAS2870 led to an upregulation of Fibulin-5 expression.
Conclusions:
- NOX1 acts as a negative modulator of Fibulin-5 in the pathogenesis of aortic dissection (AD).
- Understanding the NOX1-Fibulin-5 interaction provides insights into AD mechanisms and potential therapeutic targets.
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