ArticlePloS one2013
P21-PARP-1 pathway is involved in cigarette smoke-induced lung DNA damage and cellular senescence.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The PARP inhibitor olaparib promotes senescence in murine macrophages.GeroScience · 2026Article
- Senolytic therapy reduces inflammation in epithelial cells from COPD patients and in smoke-exposure mice.Frontiers in medicine · 2025Article
- Gene Expression in Cord Blood and Tuberculosis in Early Childhood: A Nested Case-Control Study in a South African Birth Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Article
- Article
- Revealing the pathogenic and ageing-related mechanisms of the enigmatic idiopathic pulmonary fibrosis (and chronic obstructive pulmonary disease).Current opinion in pulmonary medicine · 2022Review
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- The role of miRNAs in alveolar epithelial cells in emphysema.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021Review
- Combined EGFR1 and PARP1 Inhibition Enhances the Effect of Radiation in Head and Neck Squamous Cell Carcinoma Models.Radiation research · 2020Article
- Nicotine in Senescence and Atherosclerosis.Cells · 2020Review
- Rosiglitazone ameliorates senescence and promotes apoptosis in ovarian cancer induced by olaparib.Cancer chemotherapy and pharmacology · 2020Article
- Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model.Nutrients · 2019Article
- Cellular senescence in the lung across the age spectrum.American journal of physiology. Lung cellular and molecular physiology · 2019Review
- Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Genetic Ablation of p16American journal of respiratory cell and molecular biology · 2018Article
- Redox regulation of circadian molecular clock in chronic airway diseases.Free radical biology & medicine · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent DNA damage triggers cellular senescence, which may play an important role in the pathogenesis of cigarette smoke (CS)-induced lung diseases. Both p21(CDKN1A) (p21) and poly(ADP-ribose) polymerase-1 (PARP-1) are involved in DNA damage and repair. However, the role of p21-PARP-1 axis in regulating CS-induced lung DNA damage and cellular senescence remains unknown. We hypothesized that CS causes DNA damage and cellular senescence through a p21-PARP-1 axis. To test this hypothesis, we determined the levels of γH2AX (a marker for DNA double-strand breaks) as well as non-homologous end joining proteins (Ku70 and Ku80) in lungs of mice exposed to CS. We found that the level of γH2AX was increased, whereas the level of Ku70 was reduced in lungs of CS-exposed mice. Furthermore, p21 deletion reduced the level of γH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS. Administration of PARP-1 inhibitor 3-aminobenzamide increased CS-induced DNA damage, but lowered the levels of Ku70 and Ku80, in lungs of p21 knockout mice. Moreover, 3-aminobenzamide increased senescence-associated β-galactosidase activity, but decreased the expression of proliferating cell nuclear antigen in mouse lungs in response to CS. Interestingly, 3-aminobenzamide treatment had no effect on neutrophil influx into bronchoalveolar lavage fluid by CS. These results demonstrate that the p21-PARP-1 pathway is involved in CS-induced DNA damage and cellular senescence.
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Registered trials
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