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Recent research suggests that chronic obstructive pulmonary disease (COPD) may be a disease of accelerated aging. The senescence hypothesis of COPD pathogenesis is supported by in-vitro, in-vivo and clinical studies. The purpose of this review is to provide a comprehensive overview of the senescence hypothesis of COPD and summarize methods that are used to assess cellular aging.Accelerated aging due to exposure to cigarette smoke is hypothesized to induce rapid progression of COPD. Recent studies have shown that COPD patients have enhanced expression of senescence-associated proteins in the lung and in the peripheral circulation compared to healthy controls. Murine models of accelerated aging demonstrate spontaneous emphysematous changes in the lungs, while lungs of COPD patients demonstrate enhanced markers of senescence in fibroblasts and alveolar cells. More recently, studies of telomeres, which shorten with cellular aging, have shown that COPD patients may experience accelerated telomere attrition compared with healthy controls. However, studies to date have been relatively small and have produced heterogeneous results.The evidence for the role of accelerated aging in COPD progression is growing and senescence is one possible molecular pathway by which COPD occurs.