2014
DOI: 10.1038/cmi.2014.89
|View full text |Cite
|
Sign up to set email alerts
|

NADPH oxidases: an overview from structure to innate immunity-associated pathologies

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

10
647
0
8

Year Published

2016
2016
2022
2022

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 784 publications
(713 citation statements)
references
References 291 publications
10
647
0
8
Order By: Relevance
“…The NADPH oxidase complex catalyzes electron transfer from NADPH to molecular oxygen and thus generates superoxide, the precursor of H 2 O 2 and other ROS (29,46). Genetic defects in NADPH oxidase cause chronic granulomatous disease, an inherited primary immunodeficiency associated with autoinflammation and autoimmunity (47)(48)(49).…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…The NADPH oxidase complex catalyzes electron transfer from NADPH to molecular oxygen and thus generates superoxide, the precursor of H 2 O 2 and other ROS (29,46). Genetic defects in NADPH oxidase cause chronic granulomatous disease, an inherited primary immunodeficiency associated with autoinflammation and autoimmunity (47)(48)(49).…”
Section: Methodsmentioning
confidence: 99%
“…To test whether CD8 Treg deficiency is a feature of all inflammatory diseases, we recruited middle-aged and older patients with psoriatic arthritis (PsA), an aggressive inflammatory syndrome of the skin and the joints (28). Middleaged patients with PsA were able to generate NOX2-expressing CD8 Tregs, and patients with PsA over 60 years of age were indistinguishable from healthy older individuals (Figure 4, C-E (29,30), but it also mediates tissue damage by ROS production. When loaded with oxidation-sensitive fluorogenic probes, CD8 Tregs and nonsuppressive, freshly isolated CD8 T cells could be clearly distinguished in that only CD8 Tregs were able to produce high levels of intracellular ROS ( Figure 5, A and B).…”
Section: Cd26mentioning
confidence: 99%
“…Allergen exposure drives oxidative stress by causing airway epithelium and smooth muscle cells to produce ROS, particularly O 2 -, through activation of NADPH oxidase (4,5). Other sources of ROS include inflammatory cells like eosinophils (6), neutrophils (7), and monocytes/macrophages (8).…”
Section: Introductionmentioning
confidence: 99%
“…ROS production may increase through modulators of its expression, such as transforming growth factor β, angiotensin II, tumor necrosis factor alpha (TNF-α), and shear stress. A decrease in expression is observed in the presence of platelet-derived growth factor (PDGF), hypoxia-induced factor 1 (HIF-1), and peroxisome proliferator-activated receptor (PPAR) gamma 14,15 . Our results showed that the Nox4 gene responded with hyperexpression during IR (IRG), which was characteristic of oxidative stress ( Table 2).…”
Section: Nadph Oxidase 4 (Nox4) Genementioning
confidence: 99%
“…This protein has a high expression level in cardiac tissue, although the degree of the difference in expression between the vessels and the myocardium is unclear. NOX4 presents a differentiated pattern of ROS production following binding of NADPH to its terminal carbon, which facilitates electron transfer, and thereafter via binding of the flavin adenine dinucleotide (FAD) to two heme residues and then to molecular oxygen; this process predominately acts as a source of hydrogen peroxide (H 2 O 2 ) and, to a lesser extent, as a source of superoxide anion (O 2 -) 13,14 . ROS production may increase through modulators of its expression, such as transforming growth factor β, angiotensin II, tumor necrosis factor alpha (TNF-α), and shear stress.…”
Section: Nadph Oxidase 4 (Nox4) Genementioning
confidence: 99%