Inhaled corticosteroids reduce senescence in endothelial progenitor cells from patients with COPD.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 35027472.
- Also identified by DOI 10.1136/thoraxjnl-2020-216807 and PMC identifier 9120381.
- Licence recorded as CC BY-NC.
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Abstract
Cellular senescence contributes to the pathophysiology of chronic obstructive pulmonary disease (COPD) and cardiovascular disease. Using endothelial colony-forming-cells (ECFC), we have demonstrated accelerated senescence in smokers and patients with COPD compared with non-smokers. Subgroup analysis suggests that ECFC from patients with COPD on inhaled corticosteroids (ICS) (n=14; eight on ICS) exhibited significantly reduced senescence (Senescence-associated-beta galactosidase activity, p21<sup>CIP1</sup>), markers of DNA damage response (DDR) and IFN-γ-inducible-protein-10 compared with patients with COPD not on ICS. In vitro studies using human-umbilical-vein-endothelial-cells showed a protective effect of ICS on the DDR, senescence and apoptosis caused by oxidative stress, suggesting a protective molecular mechanism of action of corticosteroids on endothelium.
Medical subject headings
- Endothelial Progenitor Cells
- Pulmonary Disease, Chronic Obstructive