Abstract
Chronic obstructive pulmonary disease (COPD) is the important medical and social problem. According to modern concepts, COPD is a chronic inflammatory disease, macrophages play a key role in its pathogenesis. Macrophages are heterogeneous in their functions, which is largely determined by their immunometabolic profile, as well as the features of lipid homeostasis, in which the ATP binding cassette transporter A1 (ABCA1) plays an essential role. The objective of this work is the analysis of the ABCA1 protein participation and the function of reverse cholesterol transport in the pathogenesis of COPD. The expression of the ABCA1 gene in lung tissues takes the second place after the liver, which indicates the important role of the carrier in lung function. The participation of the transporter in the development of COPD consists in provision of lipid metabolism, regulation of inflammation, phagocytosis, and apoptosis. Violation of the processes in which ABCA1 is involved may be a part of the pathophysiological mechanisms, leading to the formation of a heterogeneous clinical course of the disease.
Highlights
Chronic obstructive pulmonary disease (COPD) is one of the most widespread diseases, it has great medical significance due to the high frequency of temporary and persistent disability and mortality
The increased levels of IL-6 observed in the induced sputum and lung tissue of patients with COPD [156,157] are in good agreement with the data on the reduction of the ATP binding cassette transporter A1 (ABCA1) transport function in macrophages during smoking, as well as with the fact that IL-6 is known to activate STAT3 [158]
The performed analysis of the data showed that ABCA1 can take part in various processes that are disrupted in COPD
Summary
Chronic obstructive pulmonary disease (COPD) is one of the most widespread diseases, it has great medical significance due to the high frequency of temporary and persistent disability and mortality. Inflammation in COPD is characterized by the participation of many cells and humoral factors and is believed to have local and systemic components that can be the basis for the development of comorbid diseases. Cross-links and their disruptions in the regulation of lipid metabolism, the innate immune system, and inflammation may be the key to understanding the pathophysiological bases of COPD. In this regard, information about the participation of cholesterol and its metabolic pathways in the immune response and inflammation is of considerable clinical interest. The transport function, the nature of the transported substrates and the cellular localization of the protein have determined its role in many processes and mechanisms underlying the pathogenesis of COPD
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