ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018
Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026Review
- The roles, mechanisms, and therapeutic implications of glucocorticoids in glucose and lipid metabolism.Military Medical Research · 2026Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Altered expression profile of plasma exosomal microRNAs in exclusive electronic cigarette adult users.Scientific reports · 2025Article
- Genetic diversity leads to differential inflammatory responses to cigarette smoke in mice.Physiological reports · 2025Article
- Diagnostic Challenges and Pathogenetic Differences in Biomass-Smoke-Induced versus Tobacco-Smoke-Induced COPD: A Comparative Review.Diagnostics (Basel, Switzerland) · 2024Review
- MicroRNA mediated suppression of airway lactoperoxidase by TGF-β1 and cigarette smoke promotes airway inflammation.Journal of inflammation (London, England) · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Club cell-specific telomere protection protein 1 (TPP1) protects against tobacco smoke-induced lung inflammation, xenobiotic metabolic dysregulation, and injurious responses.FASEB bioAdvances · 2024Article
- Airway Epithelium Senescence as a Driving Mechanism in COPD Pathogenesis.Biomedicines · 2023Review
- Impact of aging on immune function in the pathogenesis of pulmonary diseases: potential for therapeutic targets.Expert review of respiratory medicine · 2023Review
- Dysregulation of mitochondrial complexes and dynamics by chronic cigarette smoke exposure Utilizing MitoQC reporter mice.Mitochondrion · 2022Article
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
- Molecular clock REV-ERBα regulates cigarette smoke-induced pulmonary inflammation and epithelial-mesenchymal transition.JCI insight · 2021Article
- p16-3MR: A Novel Model to Study Cellular Senescence in Cigarette Smoke-Induced Lung Injuries.International journal of molecular sciences · 2021Article
- Perspectives on Epigenetics Alterations Associated with Smoking and Vaping.Function (Oxford, England) · 2021Review
- Prenatal Exposure to Electronic-Cigarette Aerosols Leads to Sex-Dependent Pulmonary Extracellular-Matrix Remodeling and Myogenesis in Offspring Mice.American journal of respiratory cell and molecular biology · 2020Article
- Article
- Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 Axis.Frontiers in pharmacology · 2020Article
- miR-223: A Key Regulator in the Innate Immune Response in Asthma and COPD.Frontiers in medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase 2 (HDAC2), a critical determinant of chromatin remodeling, is reduced as a consequence of oxidative stress-mediated DNA damage and impaired repair. Cigarette smoke (CS) exposure causes DNA damage and cellular senescence. However, no information is available on the role of HDAC2 in CS-induced DNA damage, stress-induced premature senescence (SIPS), and senescence-associated secretory phenotype (SASP) during the pathogenesis of chronic obstructive pulmonary disease (COPD)/emphysema. We hypothesized that CS causes persistent DNA damage and cellular senescence via HDAC2-dependent mechanisms. We used HDAC2 global knockout (KO) and HDAC2 lung epithelial cell-specific KO [Clara cell-specific HDAC2 deletion (HDAC2 CreCC10)] mice to determine whether HDAC2 is a major player in CS-induced oxidative stress, SIPS, and SASP. HDAC2 KO mice exposed to CS show exaggerated DNA damage, inflammatory response, and decline in lung function leading to airspace enlargement. Chronic CS exposure augments lung senescence-associated β-galactosidase activity in HDAC2 KO, but not in HDAC2 CreCC10 mice. HDAC2 lung epithelial cell-specific KO did not further augment CS-induced inflammatory response and airspace enlargement but instead caused an increase in lymphoid aggregate formation. Our study reveals that HDAC2 is a key player regulating CS-induced DNA damage, inflammatory response, and cellular senescence leading to COPD/emphysema.-Sundar, I. K., Rashid, K., Gerloff, J., Rangel-Moreno, J., Li, D., Rahman, I. Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.
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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.