ReviewBiomedicines2023
Airway Epithelium Senescence as a Driving Mechanism in COPD Pathogenesis.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 23 citations in OpenAlex.
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- Article
- Structural and cellular mechanisms of mucus plugging in the larger airways.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Review
- The Role of Cellular Senescence in Obstructive Airway Diseases: From Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2026Review
- Clearance of Senescent Cells by BCLAging cell · 2026Article
- Review
- Activation of STAT3 in the COPD airway epithelium.ERJ open research · 2026Article
- Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026Article
- Cleaning, Chasing and Calming: Promising Paradigms of Senotherapy in Aging-Related Diseases.International journal of biological sciences · 2026Review
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- SPG7-Mediated Regulation of mPTP and Mitochondrial Flickering in COPD: A Bioinformatics-Based Prediction of Mechanistic Framework.International journal of chronic obstructive pulmonary disease · 2026Article
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Unravelling the role of nanomedicine in attenuating inflammation, oxidative stress and cellular ageing in chronic obstructive pulmonary disease.Archives of toxicology · 2025Review
- Computational identification of key genetic drivers in COPD: A first step towards uncovering candidate biomarkers in smokers.Biochemistry and biophysics reports · 2025Article
- Senescence at the Crossroads of Lung Development and Injury.American journal of respiratory cell and molecular biology · 2025Article
- Bufei Yishen formula alleviates airway epithelial cell senescence in COPD by activating AMPK-Sirt1-FoxO3a pathway and promoting autophagy.Scientific reports · 2025Article
- Novel therapeutic strategy: Nrf2 activation in targeting senescence-related changes in chronic obstructive pulmonary disease.Journal of thoracic disease · 2025Article
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence is a state of permanent cell cycle arrest triggered by various intrinsic and extrinsic stressors. Cellular senescence results in impaired tissue repair and remodeling, loss of physiological integrity, organ dysfunction, and changes in the secretome. The systemic accumulation of senescence cells has been observed in many age-related diseases. Likewise, cellular senescence has been implicated as a risk factor and driving mechanism in chronic obstructive pulmonary disease (COPD) pathogenesis. Airway epithelium exhibits hallmark features of senescence in COPD including activation of the p53/p21WAF1/CIP1 and p16INK4A/RB pathways, leading to cell cycle arrest. Airway epithelial senescent cells secrete an array of inflammatory mediators, the so-called senescence-associated secretory phenotype (SASP), leading to a persistent low-grade chronic inflammation in COPD. SASP further promotes senescence in an autocrine and paracrine manner, potentially contributing to the onset and progression of COPD. In addition, cellular senescence in COPD airway epithelium is associated with telomere dysfunction, DNA damage, and oxidative stress. This review discusses the potential mechanisms of airway epithelial cell senescence in COPD, the impact of cellular senescence on the development and severity of the disease, and highlights potential targets for modulating cellular senescence in airway epithelium as a potential therapeutic approach in COPD.
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.