ReviewRedox biology2020
NADPH oxidases: Pathophysiology and therapeutic potential in age-associated pulmonary fibrosis.
Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 64 citations in OpenAlex.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Activation of the impaired NAMPT/SIRT7/SOD2 axis restores alveolar progenitor cell renewal in idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2026Article
- The Mechanism of NLRP3 Inflammasome Activation and Its Roles in Chronic Rhinosinusitis.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Luteoloside alleviates bleomycin-induced pulmonary fibrosis in mice via SIRT1-mediated protective effect against alveolar epithelial cell senescence.Scientific reports · 2025Article
- DNA damage response and cell fate decisions across the lifespan: from fetal development to age-related respiratory diseases.Cell & bioscience · 2025Review
- Antioxidant RuCo nanosheet attenuates capsule fibrosis in adhesive capsulitis of shoulder by p38 MAPK signaling pathway inhibition.Materials today. Bio · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Redox Biology and Insulin-like Growth Factor-Binding Protein-6: A Potential Relationship.Biology · 2025Review
- Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19.Cell communication and signaling : CCS · 2024Review
- Review
- NOX2 mediates NLRP3/ROS facilitating nasal mucosal epithelial inflammation in chronic rhinosinusitis with nasal polyps.Heliyon · 2024Article
- A nitroreductase responsive probe for early diagnosis of pulmonary fibrosis disease.Redox biology · 2024Article
- Mechanisms of Bleomycin-induced Lung Fibrosis: A Review of Therapeutic Targets and Approaches.Cell biochemistry and biophysics · 2024Review
- Cadmium-induced lung injury is associated with oxidative stress, apoptosis, and altered SIRT1 and Nrf2/HO-1 signaling; protective role of the melatonin agonist agomelatine.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
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- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress has been associated with a number of human fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). Although oxidative stress is associated with both fibrosis and aging, the precise cellular sources(s) of reactive oxygen species (ROS) that contribute to the disease pathogenesis remain poorly understood. NADPH oxidase (Nox) enzymes are an evolutionarily conserved family, where their only known function is the production of ROS. A growing body of evidence supports a link between excessive Nox-derived ROS and numerous chronic diseases (including fibrotic disease), which is most prevalent among the elderly population. In this review, we examine the evidence for Nox isoforms in the pathogenesis of IPF, and the potential to target this enzyme family for the treatment of IPF and related fibrotic disorders. A better understanding of the Nox-mediated redox imbalance in aging may be critical to the development of more effective therapeutic strategies for age-associated fibrotic disorders. Strategies aimed at specifically blocking the source(s) of ROS through Nox inhibition may prove to be more effective as anti-fibrotic therapies, as compared to antioxidant approaches. This review also discusses the potential of Nox-targeting therapeutics currently in development.
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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.