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Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease. | LitMetric

AI Article Synopsis

  • Chronic obstructive pulmonary disease (COPD) accelerates lung aging due to an increase in senescent cells that disrupt normal tissue repair and lead to inflammation through the secretion of inflammatory proteins (SASP).
  • Research indicates that cellular senescence in COPD is related to issues like telomere dysfunction, DNA damage, and oxidative stress.
  • The review examines how cellular senescence contributes to COPD's pathology and explores potential therapies that focus on targeting the signaling pathways associated with this senescence.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228143PMC
http://dx.doi.org/10.3390/medicina58060817DOI Listing

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