Cellular metabolism and mitochondrial dysfunction in chronic obstructive pulmonary disease

Abstract

Chronic obstructive pulmonary disease (COPD) is considered a typical model of accelerated aging due to the variability and systemic nature of its manifestations. The leading factor in tissue remodeling in COPD is a change or reprogramming of the cellular metabolism in response to external factors such as tobacco combustion products, biofuels, viruses, etc. Mitochondrial biology dominates the spectrum of mechanisms of tissue and cellular reprogramming in COPD. Being parasymbiotic organelles, mitochondria have a complex system of interaction with other cells of the human body and participate in both biogenesis, or formation of new organelles, and mitophagy, or elimination of defective mitochondria by the host cell. Both of these mechanisms are dysregulated in COPD.The aim of this work is to combine the accumulated research experience in the field of cellular metabolism and the role of mitochondria for in-depth COPD phenotyping depending on the metabolic reprogramming variants and for development of new therapeutic possibilities to correct the reprogramming.Conclusion. Mitochondria are key regulators of metabolism, redox homeostasis, cell survival and proliferation. These processes are controlled by various intra- and intercellular signaling pathways and reflect the COPD-associated imbalance at the level of various tissue lineages: alveolocytes, epithelial cells of the lung tissue, smooth myocytes of the respiratory tract, alveolar macrophages, striated muscle cells, mesenchymal stromal cells, progenitor cells, etc. The studies of metabolome and mitochondrial function pointed out where to look for new therapeutic options for COPD.