ReviewAmerican journal of respiratory cell and molecular biology2012
Pulmonary endothelial cell NOX.
Review in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Identification and validation of MMP1 as a biomarker associated with mitochondrial oxidative stress in liver hepatocellular carcinoma.Scientific reports · 2025Article
- Endothelial ENaC-α Restrains Oxidative Stress in Lung Capillaries in Murine Pneumococcal Pneumonia-associated Acute Lung Injury.American journal of respiratory cell and molecular biology · 2025Article
- Can ENaC "TIP" the Scales to Reduce Endothelial Reactive Oxygen Species and Vascular Leak during Pneumococcal Lung Injury?American journal of respiratory cell and molecular biology · 2025Article
- Review
- The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023Review
- Age-Related Changes in Skeletal Muscle Oxygen Utilization.Journal of functional morphology and kinesiology · 2022Review
- Inhibiting NADPH Oxidases to Target Vascular and Other Pathologies: An Update on Recent Experimental and Clinical Studies.Biomolecules · 2022Review
- Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control.Theranostics · 2021Review
- NADPH oxidase-mediated endothelial injury in HIV- and opioid-induced pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Hypoxia-induced pulmonary hypertension in type 2 diabetic mice.Pulmonary circulation · 2017Article
- Endothelial Cell Reactive Oxygen Species and CaAdvances in experimental medicine and biology · 2017Review
- The phospholipase A2 activity of peroxiredoxin 6 modulates NADPH oxidase 2 activation via lysophosphatidic acid receptor signaling in the pulmonary endothelium and alveolar macrophages.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Macrophage Migration Inhibitory Factor: A Novel Inhibitor of Apoptosis Signal-Regulating Kinase 1-p38-Xanthine Oxidoreductase-Dependent Cigarette Smoke-Induced Apoptosis.American journal of respiratory cell and molecular biology · 2016Article
- Inflammatory response and pneumocyte apoptosis during lung ischemia-reperfusion injury in an experimental pulmonary thromboembolism model.Journal of thrombosis and thrombolysis · 2015Article
- NOX signaling in molecular cardiovascular mechanisms involved in the blood pressure homeostasis.Frontiers in physiology · 2015Review
- Beneficial effects of inhaled NO on apoptotic pneumocytes in pulmonary thromboembolism model.Theoretical biology & medical modelling · 2014Article
- Downregulation of NOX4 expression by roflumilast N-oxide reduces markers of fibrosis in lung fibroblasts.Mediators of inflammation · 2013Article
- Lung oxidative damage by hypoxia.Oxidative medicine and cellular longevity · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) have profound influences on cellular homeostasis. In excess, they can potentiate the oxidation of numerous molecules, including proteins, lipids, and nucleic acids, affecting function. Furthermore, ROS-mediated oxidation of proteins can directly or indirectly modulate gene expression via effects on redox-sensitive transcription factors or via effects on phospho-relay-mediated signal transduction. In doing so, ROS impact numerous fundamental cellular processes, and have thus been implicated as critical mediators of both homeostasis and disease pathogenesis. Vascular reduced nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major contributor of ROS within the lung. The generation of ROS in the pulmonary vasculature has a pivotal role in endothelial cell (EC) activation and function. Alterations in EC phenotype contribute to vascular tone, permeability, and inflammatory responses and, thus, have been implicated in numerous diseases of the lung, including pulmonary hypertension, ischemic-reperfusion injury, and adult respiratory distress syndrome. Thus, although a detailed understanding of NOX-derived ROS in pulmonary EC biology in the context of health and disease is nascent, there is mounting evidence implicating these enzymes as critical modifiers of diseases of the lung and pulmonary circulation. The purpose of this review is to focus specifically on known as well as putative roles for pulmonary EC NOX, with attention to studies on the intact lung.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.