Cellular metabolism and mitochondrial dysfunction in chronic obstructive pulmonary disease

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