ReviewAnnals of the American Thoracic Society2017
Dealing with Stress: Defective Metabolic Adaptation in Chronic Obstructive Pulmonary Disease Pathogenesis.
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 14 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
14 citing papers in PubMed, 20 citations in OpenAlex.
- Plasma metabolomic signatures enable the diagnosis and prognosis of chronic obstructive pulmonary disease.Nature communications · 2026Article
- Epithelial QKI Protects Against Emphysema by Maintaining Mitochondrial Integrity.bioRxiv : the preprint server for biology · 2026Article
- From metabolic alterations to chronic inflammation: mechanisms and immunoregulation of metabolic reprogramming in COPD.Frontiers in immunology · 2025Review
- Botanical formulation HX110B ameliorates PPE-induced emphysema in mice via regulation of PPAR/RXR signaling pathway.PloS one · 2024Article
- The role of mitochondria in eosinophil function: implications for severe asthma pathogenesis.Frontiers in cell and developmental biology · 2024Review
- Associations between serum mitokine levels and outcomes in stable COPD: an observational prospective study.Scientific reports · 2022Observational
- Cross organelle stress response disruption promotes gentamicin-induced proteotoxicity.Cell death & disease · 2020Article
- CUL1-Mediated Organelle Fission Pathway Inhibits the Development of Chronic Obstructive Pulmonary Disease.Computational and mathematical methods in medicine · 2020Article
- Role of Metabolic Reprogramming in Pulmonary Innate Immunity and Its Impact on Lung Diseases.Journal of innate immunity · 2020Review
- Systemic Immuno-metabolic alterations in chronic obstructive pulmonary disease (COPD).Respiratory research · 2019Article
- An Updated Overview of Metabolomic Profile Changes in Chronic Obstructive Pulmonary Disease.Metabolites · 2019Review
- Roles of mitochondrial ROS and NLRP3 inflammasome in multiple ozone-induced lung inflammation and emphysema.Respiratory research · 2018Article
- Mitochondrial Quality Control in COPD and IPF.Cells · 2018Review
- Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression.Antioxidants (Basel, Switzerland) · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mitochondrion is the main site of energy production and a hub of key signaling pathways. It is also central in stress-adaptive response due to its dynamic morphology and ability to interact with other organelles. In response to stress, mitochondria fuse into networks to increase bioenergetic efficiency and protect against oxidative damage. Mitochondrial damage triggers segregation of damaged mitochondria from the mitochondrial network through fission and their proteolytic degradation by mitophagy. Post-translational modifications of the mitochondrial proteome and nuclear cross-talk lead to reprogramming of metabolic gene expression to maintain energy production and redox balance. Chronic obstructive pulmonary disease (COPD) is caused by chronic exposure to oxidative stress arising from inhaled irritants, such as cigarette smoke. Impaired mitochondrial structure and function, due to oxidative stress-induced damage, may play a key role in causing COPD. Deregulated metabolic adaptation may contribute to the development and persistence of mitochondrial dysfunction in COPD. We discuss the evidence for deregulated metabolic adaptation and highlight important areas for investigation that will allow the identification of molecular targets for protecting the COPD lung from the effects of dysfunctional mitochondria.
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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.