Key result
Hereditary Nox2 deficiency investigated for its role in ischemia-induced oxidative stress and arterial vasodilatation.
Why the study?
Animal studies suggested that Nox1 and Nox2 isoforms may control vascular function by modulating nitric oxide bioactivity, motivating evaluation in humans with hereditary Nox2 deficiency.
Answers are grounded in this paper and cite their sources.
This pilot study investigates the role of Nox2 in ischemia-induced oxidative stress and arterial vasodilatation in patients with hereditary Nox2 deficiency (X-chronic granulomatous disease).
To the Editor: Reactive oxidant species (ROS) are a family of molecules that are involved in the modulation of arterial tone via rapid degradation of nitric oxide (NO).1 NADPH oxidase is a predominant cellular source of O2−-producing enzymes.1 Four homologs of gp91phox (Nox 2) named Nox1, Nox3, Nox4, and Nox5 have been identified as components of nonphagocyte-type NADPH oxidase.2 Recent studies performed in Nox1 and Nox2 knock-out animals suggested that these Nox isoforms may be implicated in controlling vascular function via modulation of NO bioactivity.3,4 X-chronic granulomatous disease (X-CGD) is a rare primary immunodeficiency affecting the innate immunologic system; it is caused by mutations in any of the 4 genes encoding subunits of the O2− generating NADPH oxidase, resulting in defective O2− generation and intracellular killing.5 We speculated that in patients with downregulation of NADPH oxidase the …
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Violi et al. (2006) conducted a letter in Hereditary Nox2 deficiency (X-chronic granulomatous disease). Hereditary Nox2 deficiency was evaluated on Ischemia-induced oxidative stress and arterial vasodilatation.
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