ReviewAnnals of the American Thoracic Society2017
Mitochondrial Dysfunction in Pulmonary Fibrosis.
Review in Annals of the American Thoracic Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 103 citations in OpenAlex.
- Inflammasomes in respiratory diseases: from disease pathogenesis to drug development and use of multi-omics.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Engineered levothyroxine dry powder for inhalation to treat idiopathic pulmonary fibrosis.Drug delivery and translational research · 2026Article
- Article
- Danthron prevents pulmonary fibrosis through improving mitochondrial function by upregulating carboxylesterase 3.Respiratory research · 2026Article
- Cellular Senescence in Idiopathic Pulmonary Fibrosis: Molecular Mechanisms, Pathogenic Networks, and Emerging Therapeutic Targets.Diseases (Basel, Switzerland) · 2026Review
- Mitophagy promotes lung repair and regeneration by restoring epithelial metabolic fitness.Nature communications · 2026Article
- Decreased Complex I Activity in Blood lymphocytes Correlates with Idiopathic Pulmonary Fibrosis Severity.Biochemical genetics · 2026Article
- Pulmonary fibrosis in post-COVID-19: epithelial-mesenchymal transition as a key mechanism and target for therapy.Inflammopharmacology · 2026Review
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- Aging, brain-derived neurotrophic factor, and allergen-induced pulmonary responses in mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in Mice.PloS one · 2025Article
- Targeting alveolar epithelial cell metabolism in pulmonary fibrosis: Pioneering an emerging therapeutic strategy.Frontiers in cell and developmental biology · 2025Review
- Study on the Mechanism of Artesunate in Modulating AR Epithelial Injury and Th2-Type Inflammatory Status.Journal of inflammation research · 2025Article
- Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2025Review
- ACSL1 improves pulmonary fibrosis by reducing mitochondrial damage and activating PINK1/Parkin mediated mitophagy.Scientific reports · 2024Article
- Idiopathic pulmonary fibrosis (IPF): disease pathophysiology, targets, and potential therapeutic interventions.Molecular and cellular biochemistry · 2024Review
- Metabolic alterations and mitochondrial dysfunction in human airway BEAS-2B cells exposed to vanadium pentoxide.Toxicology · 2024Article
- ANT1 and the SASP: Beyond the Bioenergetic Void.American journal of respiratory cell and molecular biology · 2023Article
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Exercise Effects on Health-Related Quality of Life (HRQOL), Muscular Function, Cardiorespiratory Function, and Body Composition in Smokers: A Narrative Review.International journal of environmental research and public health · 2023Review
7 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The aging of the human population has resulted in an unprecedented increase in the incidence and prevalence of age-related diseases, including those of the lung. Idiopathic pulmonary fibrosis is a disease of aging, and is characterized by a progressive decline in lung function and high mortality. Recent studies suggest that mitochondrial dysfunction, which can accompany aging phenotypes, may contribute to the pathogenesis of idiopathic pulmonary fibrosis. In this review, we explore current evidence for mitochondrial dysfunction in alveolar epithelial cells, fibroblasts, and immune cells that participate in the fibrotic process. Further, the fates of these cell populations and the potential to target mitochondrial dysfunction as a therapeutic strategy are discussed.
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.