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ABSTRACT
Introduction: The prevalence of chronic obstructive pulmonary disease (COPD) increases exponentially with aging. Its pathogenesis, however, is not well known and aside from smoking cessation, there are no disease-modifying treatments for this disease.
Areas covered: COPD is associated with accelerating aging and aging-related diseases. In this review, we will discuss the hallmarks of aging including genomic instability, telomere attrition, epigenetic alteration, loss of proteostasis, mitochondrial dysfunction, deregulated nutrient sensing, cellular senescence, stem cell exhaustion, and altered intercellular communication, which may be involved in COPD pathogenesis.
Expert commentary: COPD and the aging process share similar molecular and cellular changes. Aging-related molecular pathways may represent novel therapeutic targets and biomarkers for COPD.
Declaration of interest
DDS has received research funding from AstraZeneca (AZ), Boehringer Ingelheim (BI), and Merck and has received honoraria for speaking engagements and/or serving on advisory boards of AZ, BI, Novartis, and Sanofi. The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewers disclosure
A reviewer on this manuscript has disclosed research funding from National Institute of Health (NIH, NHLBI), Patient-Centered Outcomes Research Institute (PCORI), COPD-Foundation, AMGEN and GE Healthcare. This reviewer has also disclosed Consulting fees from Astra Zeneca, Boehringer Ingelheim, Grifols, CSL Behring, GE Healthcare, Verona Pharma. Peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.