ReviewJournal of translational medicine2017
The pathophysiological role of mitochondrial oxidative stress in lung diseases.
Review in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 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
97 citing papers in PubMed, 191 citations in OpenAlex.
- Plasma SH Concentrations and Mortality in Patients with Newly Diagnosed Idiopathic Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial transplantation in lung diseases: From mechanisms to application prospects.Genes & diseases · 2026Review
- Effects of proton pump inhibitors on remodeling and fibrosis in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2026Article
- Inhaled nucleic acid delivery systems for the treatment of pulmonary interstitial diseases: Challenges and opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Microplastics as environmental modifiers of lung disease.EMBO molecular medicine · 2026Review
- Research Progress on the Mechanisms of High Mucus Secretion in the Airway: A Scoping Review.International journal of chronic obstructive pulmonary disease · 2026Article
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- Mesenchymal stem cell-derived exosomes: a new hope for improving asthma airway remodeling.Annals of medicine · 2025Review
- A Novel Therapeutic Target for Pediatric Pneumonia: Sestrin2.Medicina (Kaunas, Lithuania) · 2025Article
- Wildfire Exposure and Respiratory Health: A Comprehensive Review of Emerging Evidence.Tuberculosis and respiratory diseases · 2025Article
- Nanomaterials in COPD: Emerging Therapeutic and Diagnostic Frontiers with a Focus on Metal-Organic Frameworks.International journal of molecular sciences · 2025Review
- Cyclodextrin-Based Nanotransporters as a Versatile Tool to Manage Oxidative Stress-Induced Lung Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Reactive Oxygen Species: A Double-Edged Sword in the Modulation of Cancer Signaling Pathway Dynamics.Cells · 2025Review
- Imaging in animal models: bridging experimental findings and human pathophysiology.Critical care (London, England) · 2025Review
- Evaluation of the protective effect of Compound Kushen Injection against radiation‑induced lung injury in mice.Molecular medicine reports · 2025Article
- Oral toxicity assessment and the mitigation of lung carcinogenesis by phytol and α-bisabolol combination treatment in swiss albino mice: insights into redox enzyme modulation and caspase-dependent cell death mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Molecular mechanisms of lung injury from ultra high and conventional dose rate pulsed radiation based on 4D DIA proteomics study.Scientific reports · 2025Article
- Mechanisms of metabolic transition in hypertrophic cardiomyopathy.Frontiers in physiology · 2025Review
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- Mechanisms of alveolar type II epithelial cells' mitochondrial quality control during acute lung injury/acute respiratory distress syndrome: bridging the gap between oxidative stress, inflammation, and fibrosis.Frontiers in physiology · 2025Review
37 more citing papers are in PubMed but not listed here.
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
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are critically involved in reactive oxygen species (ROS)-dependent lung diseases, such as lung fibrosis, asbestos, chronic airway diseases and lung cancer. Mitochondrial DNA (mtDNA) encodes mitochondrial proteins and is more sensitive to oxidants than nuclear DNA. Damage to mtDNA causes mitochondrial dysfunction, including electron transport chain impairment and mitochondrial membrane potential loss. Furthermore, damaged mtDNA also acts as a damage-associated molecular pattern (DAMP) that drives inflammatory and immune responses. In this review, crosstalk among alveolar epithelial cells, alveolar macrophages and mitochondria is examined. ROS-related transcription factors and downstream cell signaling pathways are also discussed. We conclude that targeting oxidative stress with antioxidant agents, such as thiol molecules, polyphenols and superoxide dismutase (SOD), and promoting mitochondrial biogenesis should be considered as novel strategies for treating lung diseases that currently have no effective treatment options.
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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.