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, p21CIP1), 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.

中文翻译：

---

吸入皮质类固醇可减少 COPD 患者内皮祖细胞的衰老

细胞衰老有助于慢性阻塞性肺病 (COPD) 和心血管疾病的病理生理学。使用内皮集落形成细胞 (ECFC)，我们已经证明与非吸烟者相比，吸烟者和 COPD 患者的衰老加速。亚组分析表明，吸入皮质类固醇 (ICS) 的 COPD 患者（n = 14；ICS 有 8 名）的 ECFC 表现出显着降低的衰老（衰老相关的 β 半乳糖苷酶活性，p21CIP1）、DNA 损伤反应标志物 (DDR) 和 IFN -γ-inducible-protein-10 与未使用 ICS 的 COPD 患者相比。使用人脐静脉内皮细胞的体外研究表明，ICS 对氧化应激引起的 DDR、衰老和细胞凋亡具有保护作用，