Disease relevance of Cyba

• Angiotensin II-induced hypertrophy is potentiated in mice overexpressing p22phox in vascular smooth muscle [1].
• Letter regarding article by Becker et al, "Hyperhomocysteinemia, a cardiac metabolic disease: role of nitric oxide and the p22phox subunit of NADPH oxidase" [2].

High impact information on Cyba

• Deletion of gp91 phox did not alter p22 phox expression but severely inhibited activated O2 species production [3].
• Hemodynamic and biochemical adaptations to vascular smooth muscle overexpression of p22phox in mice [4].
• Antisense oligonucleotides against p22phox, but not sense oligonucleotides, also increased transcriptional activity of TGF-beta1 [5].
• These studies confirm that the four CGD-related phox mRNA components of NADPH oxidase are expressed early in embryonic development and the expression occurs in a consistent sequential fashion but only p22 phox protein appears in embryonic hemocytoblast [6].
• AngII infusion increased systolic blood pressure, MRV NADPH oxidase activity and expression of p22phox mRNA [7].

Biological context of Cyba

• Concurrently, candesartan increased beta-cell mass, increased staining intensity of insulin, and decreased staining intensity of components of NAD(P)H oxidase, p22phox and gp91phox, and those of oxidative stress markers in beta-cells [8].

Anatomical context of Cyba

• Moreover, before NTG exposure, ramipril treatment decreased p22phox and gp91phox (essential NADPH oxidase subunits) mRNA expression in aortas from both mice strains [9].
• In wild-type lungs, gp91 phox and p22 phox subunits are present (relative expression: macrophages > airways and veins > PASMCs) [3].

References