ReviewCells2022
Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms.
Review in Cells, 2022. 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, 13 citations in OpenAlex.
- From Airway Inflammation to Molecular Remodeling: Integrating YKL-40, MBL and Epigenetic Biomarkers in Asthma and COPD.Biomolecules · 2026Review
- Pleth variability index as a non-invasive prognostic indicator in acute exacerbation of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2026Article
- A Narrative Review of the Correlation Between Comorbidity and Acute Exacerbation of COPD Patients.International journal of chronic obstructive pulmonary disease · 2026Review
- A Combined Bioinformatics and Clinical Validation Study IdentifiesInternational journal of molecular sciences · 2025Article
- Natural Experiments: An Efficient Tool for Population Respiratory Health Evaluation.American journal of respiratory and critical care medicine · 2025Article
- Dual roles of amino acid metabolic reprogramming in chronic airway diseases and lung cancer: therapeutic opportunities and challenges.World journal of surgical oncology · 2025Review
- Association between CRP-Albumin-Lymphocyte (CALLY) index and Asthma-COPD overlap: analysis of NHANES 2015-2018 data.BMC pulmonary medicine · 2025Article
- Asthma and respiratory comorbidities.The Journal of allergy and clinical immunology · 2025Review
- Plasma Levels of CXCL9 and MCP-3 are Increased in Asthma-COPD Overlap (ACO) Patients.International journal of chronic obstructive pulmonary disease · 2025Article
- Ergosterone ameliorates RRR-induced spleen deficiency by gut microbiota-gut metabolites and P38MAPK signaling pathway.Frontiers in microbiology · 2025Article
- The Effects of a Grape Seed Procyanidin Extract on Cytochrome P450 3A4 Activity and Inflammatory Mediators in the Lungs of Heavy Active and Former Smokers.International journal of molecular sciences · 2024Article
- RNA modifications in pulmonary diseases.MedComm · 2024Review
- Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024Review
- Multifaced roles of desmoplastic reaction and fibrosis in pancreatic cancer progression: Current understanding and future directions.Cancer science · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Asthma and COPD overlap (ACO) is characterized by patients presenting with persistent airflow limitation and features of both asthma and COPD. It is associated with a higher frequency and severity of exacerbations, a faster lung function decline, and a higher healthcare cost. Systemic inflammation in COPD and asthma is driven by type 1 T helper (Th1) and Th2 immune responses, respectively, both of which may contribute to airway remodeling in ACO. ACO-related biomarkers can be classified into four categories: neutrophil-mediated inflammation, Th2 cell responses, arachidonic acid-eicosanoids pathway, and metabolites. Gene-environment interactions are key contributors to the complexity of ACO and are regulated by epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. Thus, this review focuses on the link between epigenetics and ACO, and outlines the following: (I) inheriting epigenotypes without change with environmental stimuli, or epigenetic changes in response to long-term exposure to inhaled particles plus intermittent exposure to specific allergens; (II) epigenetic markers distinguishing ACO from COPD and asthma; (III) potential epigenetic drugs that can reverse oxidative stress, glucocorticoid insensitivity, and cell injury. Improved understanding of the epigenetic regulations holds great value to give deeper insight into the mechanisms, and clarify their implications for biomedical research in ACO.
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.