Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease
- PMID: 35744080
- PMCID: PMC9228143
- DOI: 10.3390/medicina58060817
Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease
Abstract
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.
Keywords: aging; chronic obstructive pulmonary disease; cigarette smoke; senescence.
Conflict of interest statement
The authors declare no conflict of interest.
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- Vogelmeier C.F., Criner G.J., Martinez F.J., Anzueto A., Barnes P.J., Bourbeau J., Celli B.R., Chen R., Decramer M., Fabbri L.M., et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2017 Report. GOLD Executive Summary. Am. J. Respir. Crit. Care Med. 2017;195:557–582. doi: 10.1164/rccm.201701-0218PP. - DOI - PubMed
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