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Association of Clonal Hematopoiesis of Indeterminate Potential with Inflammatory Gene Expression in Patients with COPD

MPG-Autoren
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Mansouri,  Siavash
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Savai,  Rajkumar
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Avci,  Edibe
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Diaz-Pina,  Gabriela
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Padmasekar,  Manju
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Looso,  Mario
Bioinformatics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Wilhelm,  Jochen
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Seeger,  Werner
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Pullamsetti,  Soni S.
Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Zitation

Kuhnert, S., Mansouri, S., Rieger, M. A., Savai, R., Avci, E., Diaz-Pina, G., et al. (2022). Association of Clonal Hematopoiesis of Indeterminate Potential with Inflammatory Gene Expression in Patients with COPD. CELLS, 11(13): 2121. doi:10.3390/cells11132121.


Zitierlink: https://hdl.handle.net/21.11116/0000-000A-BFF9-7
Zusammenfassung
Chronic obstructive pulmonary disease (COPD) is a disease with an inflammatory phenotype with increasing prevalence in the elderly. Expanded population of mutant blood cells carrying somatic mutations is termed clonal hematopoiesis of indeterminate potential (CHIP). The association between CHIP and COPD and its relevant effects on DNA methylation in aging are mainly unknown. Analyzing the deep-targeted amplicon sequencing from 125 COPD patients, we found enhanced incidence of CHIP mutations (similar to 20%) with a predominance of DNMT3A CHIP-mediated hypomethylation of Phospholipase D Family Member 5 (PLD5), which in turn is positively correlated with increased levels of glycerol phosphocholine, pro-inflammatory cytokines, and deteriorating lung function.