The NADPH oxidase NOX4 regulates redox and metabolic homeostasis preventing HCC progression [PDF]
Loss of NOX4 in HCC tumor cells induces metabolic reprogramming in a Nrf2/MYC‐dependent manner to promote HCC progression. Abstract Background and Aims The NADPH oxidase NOX4 plays a tumor‐suppressor function in HCC. Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in ...
Irene Peñuelas‐Haro +14 more
wiley +2 more sources
Regulation of Monocyte Adhesion and Migration by Nox4 [PDF]
We showed that metabolic disorders promote thiol oxidative stress in monocytes, priming monocytes for accelerated chemokine-induced recruitment, and accumulation at sites of vascular injury and the progression of atherosclerosis. The aim of this study was to identify both the source of reactive oxygen species (ROS) responsible for thiol oxidation in ...
Chi Fung Lee +3 more
openaire +5 more sources
Role of the TSPO–NOX4 axis in angiogenesis in glioblastoma
Objective: Angiogenesis is a pathological feature of glioblastoma. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) is a vital source of reactive oxygen species (ROS) related to angiogenesis.
Hongxiang Jiang +5 more
doaj +3 more sources
NADPH oxidase 4 (Nox4) deletion accelerates liver regeneration in mice [PDF]
Liver is a unique organ in displaying a reparative and regenerative response after acute/chronic damage or partial hepatectomy, when all the cell types must proliferate to re-establish the liver mass.
M. Herranz-Itúrbide +11 more
doaj +2 more sources
Role of Nox4 in murine models of kidney disease
Nox4 is a hydrogen peroxide-producing NADPH oxidase highly expressed in the kidney which has been linked to epithelial cell injury and diabetic-induced cellular dysfunction in cultured cells. The role of the enzyme for renal pathology in vivo, however, is unclear.
Babelova, Andrea +11 more
openaire +4 more sources
NOX4-mediated astrocyte ferroptosis in Alzheimer’s disease
AbstractThis study investigates NADPH oxidase 4 (NOX4) involvement in iron-mediated astrocyte cell death in Alzheimer’s Disease (AD) using single-cell sequencing data and transcriptomes. We analyzed AD single-cell RNA sequencing data, identified astrocyte marker genes, and explored biological processes in astrocytes.
Yasenjiang Maimaiti +5 more
openaire +4 more sources
Strategies Aimed at Nox4 Oxidase Inhibition Employing Peptides from Nox4 B-Loop and C-Terminus and p22phox N-Terminus: An Elusive Target [PDF]
Although NADPH oxidase 4 (Nox4) is the most abundant Nox isoform in systemic vascular endothelial and smooth muscle cells, its function in the vascular tissue is not entirely known.
Gábor Csányi, Patrick J. Pagano
doaj +2 more sources
NOX4–TIM23 interaction regulates NOX4 mitochondrial import and metabolic reprogramming
Pulmonary fibrosis is a progressive lung disease characterized by macrophage activation. Asbestos-induced expression of nicotinamide adenine dinucleotide phosphate hydrogen oxidase 4 (NOX4) in lung macrophages mediates fibrotic progression by the generation of mitochondrial reactive oxygen species (ROS), modulating mitochondrial biogenesis, and ...
Jyotsana Pandey +7 more
openaire +2 more sources
The Radioprotective Effect of Magnesium Sulfate and Vitamin A on Radiation-induced Micronuclei and the Expression of NOX4 in Bone Marrow Cells of Mice [PDF]
Background: Radioprotectors are used to neutralize the effects of free radicals caused by ionization radiation. In this study, the radioprotective effects of magnesium sulfate and vitamin A on bone marrow cells of mice were evaluated by micronucleus ...
Mohammad Mirdoraghi +5 more
doaj +1 more source
Nox4, one of the 7 isoforms of the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase family that generate reactive oxygen species, was first identified in the early 2000s in kidneys.1 Nox4 was originally described as an oxygen sensor and regulator of kidney cell growth and because of its renal abundance was termed “renox.”1 It soon became ...
Touyz, R.M., Montezano, A.C.
openaire +3 more sources

