ReviewCellular and molecular life sciences : CMLS2012
NOX enzymes: potential target for the treatment of acute lung injury.
Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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
37 citing papers in PubMed, 68 citations in OpenAlex.
- NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.Frontiers in immunology · 2026Article
- Inhibition of S100A12 Attenuates LPS-induced Endothelial Barrier Dysfunction in HPMECs through the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Article
- Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Time-Dependent Oxidative Alterations in Plasma and Lung Tissue after Meconium Aspiration in a Rabbit Model.Antioxidants (Basel, Switzerland) · 2022Article
- Effects of Corilagin on Lipopolysaccharide-Induced Acute Lung Injury via Regulation of NADPH Oxidase 2 and ERK/NF-Biology · 2022Article
- Polyphenols-Rich Fraction fromPharmaceutics · 2022Article
- Profiling Distinctive Inflammatory and Redox Responses to Hydrogen Sulfide in Stretched and Stimulated Lung Cells.Antioxidants (Basel, Switzerland) · 2022Article
- NR4A1 Promotes LPS-Induced Acute Lung Injury through Inhibition of Opa1-Mediated Mitochondrial Fusion and Activation of PGAM5-Related Necroptosis.Oxidative medicine and cellular longevity · 2022Article
- Oxidative Stress-Related Mechanisms in SARS-CoV-2 Infections.Oxidative medicine and cellular longevity · 2022Review
- Friend or Foe? The Roles of Antioxidants in Acute Lung Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells.BMC pulmonary medicine · 2021Article
- Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NFκB Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Hydrogen Sulfide Exerts Anti-oxidative and Anti-inflammatory Effects in Acute Lung Injury.Inflammation · 2018Article
- Protective Effect of Jianpiyifei II Granule against Chronic Obstructive Pulmonary Disease via NF-Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Early application of low-dose glucocorticoid improves acute respiratory distress syndrome: A meta-analysis of randomized controlled trials.Experimental and therapeutic medicine · 2017Article
- Dysregulated Nox4 ubiquitination contributes to redox imbalance and age-related severity of acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Hydrogen Sulfide Prevents Formation of Reactive Oxygen Species through PI3K/Akt Signaling and Limits Ventilator-Induced Lung Injury.Oxidative medicine and cellular longevity · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), is characterized by acute inflammation, disruption of the alveolar-capillary barrier, and in the organizing stage by alveolar pneumocytes hyperplasia and extensive lung fibrosis. The cellular and molecular mechanisms leading to the development of ALI/ARDS are not completely understood, but there is evidence that reactive oxygen species (ROS) generated by inflammatory cells as well as epithelial and endothelial cells are responsible for inflammatory response, lung damage, and abnormal repair. Among all ROS-producing enzymes, the members of NADPH oxidases (NOXs), which are widely expressed in different lung cell types, have been shown to participate in cellular processes involved in the maintenance of lung integrity. It is not surprising that change in NOXs' expression and function is involved in the development of ALI/ARDS. In this context, the use of NOX inhibitors could be a possible therapeutic perspective in the management of this syndrome. In this article, we summarize the current knowledge concerning some cellular aspects of NOXs localization and function in the lungs, consider their contribution in the development of ALI/ARDS and discuss the place of NOX inhibitors as potential therapeutical target.
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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.