A tale as old as time - the importance of accelerated lung aging in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is progressive in nature and predominantly affects older individuals. Lung function decline is a typical part of the aging process, characterized by gradual loss of lung mechanics, airway remodeling, persistent low-grade inflammation of the airways, compromised epithelial barrier function, and impaired immune responses over time.

The pathology of the senile lung is advanced in patients with COPD, whereby genomic damages contribute to structural defects and cellular dysfunction. Primary, antagonistic, and integrative hallmarks of aging are accelerated in COPD, potentiated by cumulative injury sustained from repeated environmental exposures and the interaction with comorbidities. Identification of epigenetic profiles in COPD indicates how cellular processes contribute to the advancement of biological age. Epigenetic abnormalities unique to COPD subpopulations occur in individuals who are immunodeficient, and often experience early onset and increased severity of COPD.

Accelerated aging processes indicated by epigenetic and other biomarkers may be a promising avenue for early detection, prevention, and subsequent management of COPD. Understanding risk factors contributing to progressive lung function decline and implementation of mitigation strategies such as cessation of smoking, repurposing existing pharmacotherapeutics and development of novel therapies may slow age-related pathologies in COPD. [Figure: see text].