ArticleAmerican journal of respiratory cell and molecular biology2015
Disruption of Sirtuin 1-Mediated Control of Circadian Molecular Clock and Inflammation in Chronic Obstructive Pulmonary Disease.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 90 citations in OpenAlex.
- Cryptochrome Loss Drives COPD-like Lung Pathology through Disrupted Alveolar Epithelial Proliferation and Immune Homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Circadian clock regulation in lung health and disease: molecular mechanisms and therapeutic opportunities.EXCLI journal · 2026Review
- Integrative multi-omics and machine learning identify CHRNA1 putative circadian-immune hub in COPD.PloS one · 2026Article
- Targeting Circadian Rhythm for the Regulation of Skin Collagen Metabolism.Journal of cosmetic dermatology · 2026Article
- The lung-muscle axis in COPD: a conceptual framework integrating evidence, mechanisms, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Nicotine influence on cerebrovascular and neurocognitive function with in utero electronic cigarette exposure.The Journal of physiology · 2025Article
- Review
- Perturbation of the circadian clock in chronic diseases involving organ fibrosis.The Journal of clinical investigation · 2025Review
- Bubble Trouble: Epithelial Extracellular Vesicles and Their microRNA Mischief in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Peptidylarginine Deiminase 4 Deficiency Suppresses Neutrophil Extracellular Trap Formation and Ameliorates Elastase-Induced Emphysema in Mouse Lung.International journal of molecular sciences · 2025Article
- A network of pro-inflammatory genes repressed by clock signalling in bronchial epithelium.ERJ open research · 2025Article
- Emerging trends and hotspots in chronic obstructive pulmonary disease and oxidative stress: a bibliometric and visualized analysis from 2010 to 2024.Journal of thoracic disease · 2025Article
- Role of circadian transcription factor REV-ERB in cardiovascular diseases: a review.Frontiers in cardiovascular medicine · 2025Review
- Article
- Core circadian transcription factor Bmal1 mediates β cell response and recovery from pro-inflammatory injury.iScience · 2024Article
- Analysis of Key Genes and miRNA-mRNA Networks Associated with Glucocorticoids Treatment in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- Hypoxia Induces Alterations in the Circadian Rhythm in Patients with Chronic Respiratory Diseases.Cells · 2023Review
- Acute and Repeated Ozone Exposures Differentially Affect Circadian Clock Gene Expression in Mice.Advanced biology · 2023Article
- Targeting Rev-Erbα to protect against ischemia-reperfusion-induced acute lung injury in rats.Respiratory research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is the fourth most common cause of death, and it is characterized by abnormal inflammation and lung function decline. Although the circadian molecular clock regulates inflammatory responses, there is no information available regarding the impact of COPD on lung molecular clock function and its regulation by sirtuin 1 (SIRT1). We hypothesize that the molecular clock in the lungs is disrupted, leading to increased inflammatory responses in smokers and patients with COPD and its regulation by SIRT1. Lung tissues, peripheral blood mononuclear cells (PBMCs), and sputum cells were obtained from nonsmokers, smokers, and patients with COPD for measurement of core molecular clock proteins (BMAL1, CLOCK, PER1, PER2, and CRY1), clock-associated nuclear receptors (REV-ERBα, REV-ERBβ, and RORα), and SIRT1 by immunohistochemistry, immunofluorescence, and immunoblot. PBMCs were treated with the SIRT1 activator SRT1720 followed by LPS treatment, and supernatant was collected at 6-hour intervals. Levels of IL-8, IL-6, and TNF-α released from PBMCs were determined by ELISA. Expression of BMAL1, PER2, CRY1, and REV-ERBα was reduced in PBMCs, sputum cells, and lung tissues from smokers and patients with COPD when compared with nonsmokers. SRT1720 treatment attenuated LPS-mediated reduction of BMAL1 and REV-ERBα in PBMCs from nonsmokers. Additionally, LPS differentially affected the timing and amplitude of cytokine (IL-8, IL-6, and TNF-α) release from PBMCs in nonsmokers, smokers, and patients with COPD. Moreover, SRT1720 was able to inhibit LPS-induced cytokine release from cultured PBMCs. In conclusion, disruption of the molecular clock due to SIRT1 reduction contributes to abnormal inflammatory response in smokers and patients with COPD.
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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 Socratic graph.