ArticleFree radical biology & medicine2007
Nox2 regulates endothelial cell cycle arrest and apoptosis via p21cip1 and p53.
Article in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Investigation of the Effects of a Novel NOX2 Inhibitor, GLX7013170, against Glutamate Excitotoxicity and Diabetes Insults in the Retina.Pharmaceuticals (Basel, Switzerland) · 2024Article
- NOX2 and NOX5 are increased in cardiac microvascular endothelium of deceased COVID-19 patients.International journal of cardiology · 2023Article
- Role of Phosphoinositide 3-Kinase in Regulation of NOX-Derived Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2022Review
- L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2022Article
- A risk model of 10 aging-related genes for predicting survival and immune response in triple-negative breast cancer.Cancer medicine · 2022Article
- Capillaries as a Therapeutic Target for Heart Failure.Journal of atherosclerosis and thrombosis · 2022Article
- Chronic exposure to tramadol induces cardiac inflammation and endothelial dysfunction in mice.Scientific reports · 2021Article
- Induced Trf2 deletion leads to aging vascular phenotype in mice associated with arterial telomere uncapping, senescence signaling, and oxidative stress.Journal of molecular and cellular cardiology · 2019Article
- The matricellular protein TSP1 promotes human and mouse endothelial cell senescence through CD47 and Nox1.Science signaling · 2017Article
- Aging-associated metabolic disorder induces Nox2 activation and oxidative damage of endothelial function.Free radical biology & medicine · 2017Article
- NADPH oxidase in brain injury and neurodegenerative disorders.Molecular neurodegeneration · 2017Review
- p22phox C242T Single-Nucleotide Polymorphism Inhibits Inflammatory Oxidative Damage to Endothelial Cells and Vessels.Circulation · 2016Article
- Effects of n-3 polyunsaturated fatty acids high fat diet intervention on the synthesis of hepatic high-density lipoprotein cholesterol in obesity-insulin resistance rats.Lipids in health and disease · 2016Article
- NADPH oxidases: key modulators in aging and age-related cardiovascular diseases?Clinical science (London, England : 1979) · 2016Review
- Role of pulmonary microvascular endothelial cell apoptosis in murine sepsis-induced lung injury in vivo.Respiratory research · 2015Article
- Oxidative stress, redox signalling and endothelial dysfunction in ageing-related neurodegenerative diseases: a role of NADPH oxidase 2.British journal of clinical pharmacology · 2014Review
- Ethers and esters derived from apocynin avoid the interaction between p47phox and p22phox subunits of NADPH oxidase: evaluation in vitro and in silico.Bioscience reports · 2013Article
- Mitochondria and reactive oxygen species: physiology and pathophysiology.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial cells (EC) express constitutively two major isoforms (Nox2 and Nox4) of the catalytic subunit of NADPH oxidase, which is a major source of endothelial reactive oxygen species. However, the individual roles of these Noxes in endothelial function remain unclear. We have investigated the role of Nox2 in nutrient deprivation-induced cell cycle arrest and apoptosis. In proliferating human dermal microvascular EC, Nox2 mRNA expression was low relative to Nox4 (Nox2:Nox4 approximately 1:13), but was upregulated 24 h after starvation and increased to 8+/-3.5-fold at 36 h of starvation. Accompanying the upregulation of Nox2, there was a 2.28+/-0.18-fold increase in O2.- production, a dramatic induction of p21cip1 and p53, cell cycle arrest, and the onset of apoptosis (all p<0.05). All these changes were inhibited significantly by in vitro deletion of Nox2 expression and in coronary microvascular EC isolated from Nox2 knockout mice. In Nox2 knockout cells, although there was a 3.8+/-0.5-fold increase in Nox4 mRNA expression after 36 h of starvation (p<0.01), neither O2.- production nor the p21cip1 or p53 expression was increased significantly and only 0.46% of cells were apoptotic. In conclusion, Nox2-derived O2.-, through the modulation of p21cip1 and p53 expression, participates in endothelial cell cycle regulation and apoptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.