ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Critical Biological Functions and Clinical Implications of Epigenetic-Related Candidate Biomarkers in Chronic Obstructive Pulmonary Disease: Integrated Machine Learning Screening and Basic Experimental Validation.International journal of chronic obstructive pulmonary disease · 2026Article
- Bladder neck contracture: incidence, mechanisms, and therapeutic advances.Annals of medicine and surgery (2012) · 2025Review
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- Consecutive Hypoxia Decreases Expression ofFrontiers in cell and developmental biology · 2020Article
- Hypoxia signaling in human diseases and therapeutic targets.Experimental & molecular medicine · 2019Review
- Adenosine and hyaluronan promote lung fibrosis and pulmonary hypertension in combined pulmonary fibrosis and emphysema.Disease models & mechanisms · 2019Article
- Cleavage factor 25 deregulation contributes to pulmonary fibrosis through alternative polyadenylation.The Journal of clinical investigation · 2019Article
- dCK negatively regulates the NRF2/ARE axis and ROS production in pancreatic cancer.Cell proliferation · 2018Article
- Hypoxia downregulates protein S expression.Blood · 2018Article
- The Role of Deoxycytidine Kinase (dCK) in Radiation-Induced Cell Death.International journal of molecular sciences · 2016Article
- Aeroallergen Der p 2 induces apoptosis of bronchial epithelial BEAS-2B cells via activation of both intrinsic and extrinsic pathway.Cell & bioscience · 2015Article
- Hypoxia-induced deoxycytidine kinase contributes to epithelial proliferation in pulmonary fibrosis.American journal of respiratory and critical care medicine · 2014Article
- Structural characterization of new deoxycytidine kinase inhibitors rationalizes the affinity-determining moieties of the molecules.Acta crystallographica. Section D, Biological crystallography · 2014Article
- Using a non-invasive assessment of lung injury in a murine model of acute lung injury.BMJ open respiratory research · 2014Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by persistent inflammation and tissue remodeling and is a leading cause of death in the United States. Increased apoptosis of pulmonary epithelial cells is thought to play a role in COPD development and progression. Identification of signaling pathways resulting in increased apoptosis in COPD can be used in the development of novel therapeutic interventions. Deoxyadenosine (dAdo) is a DNA breakdown product that amplifies lymphocyte apoptosis by being phosphorylated to deoxyadenosine triphosphate (dATP). dAdo is maintained at low levels by adenosine deaminase (ADA). This study demonstrated that mice lacking ADA developed COPD manifestations in association with elevated dAdo and dATP levels and increased apoptosis in the lung. Deoxycitidine kinase (DCK), a major enzyme for dAdo phosphorylation, was up-regulated in mouse and human airway epithelial cells in association with air-space enlargement. Hypoxia was identified as a novel regulator of DCK, and inhibition of DCK resulted in diminished dAdo-mediated apoptosis in the lungs. Our results suggest that activating the dAdo-DCK-dATP pathway directly results in increased apoptosis in the lungs of mice with air-space enlargement and suggests a novel therapeutic target for the treatment of COPD.
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