Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY 11203, USA.
Section of Pulmonary, Critical Care and Sleep Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Medicina (Kaunas). 2022 Jun 17;58(6):817. doi: 10.3390/medicina58060817.
Chronic obstructive pulmonary disease (COPD) is recognized as a disease of accelerated lung aging. Over the past two decades, mounting evidence suggests an accumulation of senescent cells within the lungs of patients with COPD that contributes to dysregulated tissue repair and the secretion of multiple inflammatory proteins, termed the senescence-associated secretory phenotype (SASP). Cellular senescence in COPD is linked to telomere dysfunction, DNA damage, and oxidative stress. This review gives an overview of the mechanistic contributions and pathologic consequences of cellular senescence in COPD and discusses potential therapeutic approaches targeting senescence-associated signaling in COPD.
慢性阻塞性肺疾病(COPD)被认为是一种加速肺部衰老的疾病。在过去的二十年中,越来越多的证据表明,COPD 患者肺部衰老细胞的积累导致组织修复失调和多种炎症蛋白的分泌,这些蛋白被称为衰老相关分泌表型(SASP)。COPD 中的细胞衰老与端粒功能障碍、DNA 损伤和氧化应激有关。本文综述了细胞衰老在 COPD 中的机制贡献和病理后果,并讨论了针对 COPD 中衰老相关信号的潜在治疗方法。