ArticleFrontiers in medicine2025
Senolytic therapy reduces inflammation in epithelial cells from COPD patients and in smoke-exposure mice.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- The right time, the right cell: the potential for precision senotherapy in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Clearance of Senescent Cells by BCLAging cell · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Microgravity Therapy as Treatment for Decelerated Aging and Successful Longevity.International journal of molecular sciences · 2025Review
- Small airway disease as a key factor in COPD: new perspectives and insights.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Chronic obstructive pulmonary disease (COPD) is a disease of accelerated lung aging, with increased numbers of senescent cells found within the COPD Lung. Senescent cells may drive pathology by causing defective tissue repair and driving chronic inflammation via the release of inflammatory mediators known as the senescence-associated secretory phenotype (SASP). Senolytics are a new class of drugs that selectively remove senescent cells but have not previously been studied in COPD. We examined whether senescent cells are maintained during differentiation of COPD airway epithelial cells at the air-liquid interface and examined the role of the senolytic combination of dasatinib and quercetin on these cells and in a smoke-exposure mouse model. Methods: Non-smoker and COPD bronchial epithelial cells were differentiated at air-liquid interface (ALI). Senescence markers (p16 Results: Increased senescence markers were maintained in COPD ALI epithelium when differentiated at air-liquid interface, and treatment with D + Q reduced senescence markers, proteases, and Th2 cytokines. Therapeutic oral treatment of D + Q to CS-exposed mice reduced senescence burden while reducing inflammatory cell infiltrates and mouse CXCL1. Conclusion: COPD subjects show increased airway epithelial senescence, and these cells can be cleared therapeutically using the senolytic cocktail of D + Q, reducing broad-spectrum pulmonary inflammation
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