ArticleAmerican journal of respiratory and critical care medicine2012
Retinoic acid-related orphan receptor-α is induced in the setting of DNA damage and promotes pulmonary emphysema.
Article in American journal of respiratory and critical care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Identification of potential susceptibility loci for non-small cell lung cancer through whole genome sequencing in circadian rhythm genes.Scientific reports · 2025Article
- The Role of Retinoic-Acid-Related Orphan Receptor (RORs) in Cellular Homeostasis.International journal of molecular sciences · 2024Review
- Hypoxia Induces Alterations in the Circadian Rhythm in Patients with Chronic Respiratory Diseases.Cells · 2023Review
- Circadian Disruption in Night Shift Work and Its Association with Chronic Pulmonary Diseases.Advanced biology · 2023Review
- Article
- Circadian clock molecule REV-ERBα regulates lung fibrotic progression through collagen stabilization.Nature communications · 2023Article
- Circadian molecular clock disruption in chronic pulmonary diseases.Trends in molecular medicine · 2022Review
- The role of retinoid-related orphan receptor-α in cigarette smoke-induced autophagic response.Respiratory research · 2022Article
- Molecular clock REV-ERBα regulates cigarette smoke-induced pulmonary inflammation and epithelial-mesenchymal transition.JCI insight · 2021Article
- Cigarette smoke exposure enhances transforming acidic coiled-coil-containing protein 2 turnover and thereby promotes emphysema.JCI insight · 2020Article
- Nuclear Receptors in Asthma: Empowering Classical Molecules Against a Contemporary Ailment.Frontiers in immunology · 2020Review
- RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia.BMC genomics · 2019Article
- Total particulate matter concentration skews cigarette smoke's gene expression profile.ERJ open research · 2016Article
- APO-9'-Fucoxanthinone Extracted from Undariopsis peteseniana Protects Oxidative Stress-Mediated Apoptosis in Cigarette Smoke-Exposed Human Airway Epithelial Cells.Marine drugs · 2016Article
- Candidate SNP Markers of Chronopathologies Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters.BioMed research international · 2016Article
- Disruption of Sirtuin 1-Mediated Control of Circadian Molecular Clock and Inflammation in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2015Article
- Circadian molecular clock in lung pathophysiology.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Genetic variations in RORα are associated with chronic obstructive pulmonary disease.Journal of human genetics · 2014Article
- Molecular processes that drive cigarette smoke-induced epithelial cell fate of the lung.American journal of respiratory cell and molecular biology · 2014Review
- P21-PARP-1 pathway is involved in cigarette smoke-induced lung DNA damage and cellular senescence.PloS one · 2013Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleThe discovery that retinoic acid-related orphan receptor (Rora)-α is highly expressed in lungs of patients with COPD led us to hypothesize that Rora may contribute to the pathogenesis of emphysema.
objectivesTo determine the role of Rora in smoke-induced emphysema.
methodsCigarette smoke extract in vitro and elastase or cigarette smoke exposure in vivo were used to model smoke-related cell stress and airspace enlargement. Lung tissue from patients undergoing lung transplantation was examined for markers of DNA damage and Rora expression. MEASUREMENTS AND MAIN
resultsRora expression was induced by cigarette smoke in mice and in cell culture. Gene expression profiling of Rora-null mice exposed to cigarette smoke demonstrated enrichment for genes involved in DNA repair. Rora expression increased and Rora translocated to the nucleus after DNA damage. Inhibition of ataxia telangiectasia mutated decreased the induction of Rora. Gene silencing of Rora attenuated apoptotic cell death in response to cigarette smoke extract, whereas overexpression of Rora enhanced apoptosis. Rora-deficient mice were protected from elastase and cigarette smoke induced airspace enlargement. Finally, lungs of patients with COPD showed evidence of increased DNA damage even in the absence of active smoking.
conclusionsTaken together, these findings suggest that DNA damage may contribute to the pathogenesis of emphysema, and that Rora has a previously unrecognized role in cellular responses to genotoxicity. These findings provide a potential link between emphysema and features of premature ageing, including enhanced susceptibility to lung cancer.
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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 Socratic graph.