Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genetic Deletion of NADPH Oxidase 1 Rescues Microvascular Function in Mice With Metabolic Disease

7 Jul 2017

Abstract excerpt

Rationale: Early vascular changes in metabolic disease that precipitate the development of cardiovascular complications are largely driven by reactive oxygen species accumulation, yet the extent to which excess reactive oxygen species derive from specific NADPH oxidase isoforms remains ill defined. Objective: Identify the role of Nox1 in the development of microvascular dysfunction in metabolic disease. Methods...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Microbial metabolism and enzyme function
Share to Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Share to Nitric Oxide and Endothelin Effects

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 28684629
DOI: 10.1161/circresaha.116.309965

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic Deletion of NADPH Oxidase 1 Rescues Microvascular Function in Mice With Metabolic DiseasePMID 28684629Read ↗

The NADPH organizers NoxO1 and p47phox are both mediators of diabetes-induced vascular dysfunction in miceSemantic proximity Read ↗

Nox4 genetic inhibition in experimental hypertension and metabolic syndrome.Semantic proximity Read ↗

Toll-like receptor 4 mutation protects obese mice against endothelial dysfunction by decreasing NADPH oxidase isoforms 1 and 4.Semantic proximity Read ↗

Nox2-derived superoxide contributes to cerebral vascular dysfunction in diet-induced obesity.Semantic proximity Read ↗

NOX5-induced uncoupling of endothelial NO synthase is a causal mechanism and theragnostic target of an age-related hypertension endotypeSemantic proximity Read ↗

Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1Semantic proximity Read ↗

Reduced atherosclerotic burden in subjects with genetically determined low oxidative stress.Semantic proximity Read ↗

Mitochondrial dysfunction and metabolic reprogramming induce macrophage pro-inflammatory phenotype switch and atherosclerosis progression in aging.Semantic proximity Read ↗

[NO, a major regulator of metabolic and cardiovascular homeostasis].Semantic proximity Read ↗

Unchanged NADPH Oxidase Activity in Nox1-Nox2-Nox4 Triple Knockout Mice: What Do NADPH-Stimulated Chemiluminescence Assays Really Detect?Semantic proximity Read ↗

Toll-Like Receptor 2 (TLR2) Knockout Abrogates Diabetic and Obese Phenotypes While Restoring Endothelial Function via Inhibition of NOX1.Semantic proximity Read ↗

The nitrite reductase activity of xanthine oxidoreductase sustains cardiovascular healthSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.