ABSTRACT
Chronic obstructive pulmonary disease (COPD) is a disease with typical features of premature aging. Modern theories of the pathogenesis of COPD include a number of interrelated concepts that dominate in different time periods. In this work, based on the analysis of the results of our own and published scientific studies, it is demonstrated that the mitochondria-mediated component seems to be the link of most of the recognized theories of the pathogenesis of COPD as a model of early premature aging. The issues of mitochondrial involvement in the pathogenesis of COPD are actively studied, but are not fully understood and do not always have an unambiguous interpretation. The paper systematizes information on the contribution of mitochondrial dysfunction to various aspects of the pathogenesis of COPD, including the relationship between inflammation, hypoxia, oxidative stress, protease imbalance, damage to tissue and cellular phenotype with reprogramming of metabolism and accumulation of a pool of cells with an «aged¼ phenotype. Observations suggest that mitochondrial dysfunction may be a key factor contributing to the initiation and progression of COPD, the accumulation of systemic effects, the formation of comorbidity, and premature aging. The argumentation of this concept provides an evidence-based basis for the development of promising, pathogenetically substantiated targeted strategies for the prevention and control of COPD at the topical and systemic levels.
