It is well known that chronic obstructive pulmonary disease (COPD) and arterial hypertension (AH) are multifactorial diseases that develop as a result of complex interactions between genetic and environmental factors. Both internal and external factors can cause the activation of apoptosis, which is considered to be the key factor in the accelerated degradation and death of cells, leading to structural and functional disorders in organs. Apoptosis processes are initiated in the cells of affected organs long before the clinical manifestations of the disease become noticeable. Research and study of the triggering factors and pathobiology of apoptosis in AH and COPD can help to optimise screening programmes for the detection of these diseases in the early preclinical stages and develop new effective targeted treatment regimens based on blocking individual apoptosis pathways in cells.

The aim of the study is to investigate the characteristics of the synthesis, metabolism and regulation of molecules, receptors and ligands involved in apoptosis in patients with COPD and AH.

Materials and methods. For a systematic review of the literature, reviewed scientific articles indexed in leading scientometric databases (PubMed, Scopus, Google Scholar, and Web of Science) were used.

Results. Apoptosis is a complex and multi-component process of programmed cell death. It has been proven that the processes of apoptosis in vascular endothelial cells, bronchial epithelial cells, and smooth muscle cells of the vascular and bronchial walls are significantly accelerated and scaled up in conditions of comorbid COPD and AH. Various molecules, ligands, and receptors are involved in the cascade of apoptotic changes, namely caspases 3, 7, 8, and 9, active forms of oxygen, calcium-dependent proteases, cytochrome C, parkin-4, Bcl-2 family proteins, apoptosis-related protein activator factor 1 (APAF-1), heat shock proteins, tumour necrosis factor, Fas ligand, Bax and p53 proteins, and soluble messenger proteins such as MFG-E8.

Conclusions. There is a correlation between the dynamics of markers of apoptotic processes on the one hand and the severity of respiratory and haemodynamic disorders in COPD comorbidity with AH on the other. A detailed study of the mechanisms of initiation and regulation of neutrophil apoptosis involving cysteine proteases and other markers of apoptosis in patients with comorbid COPD and AH is a promising area of current research. Such data may form the basis for the correction of therapeutic regimens and allow for the optimisation of treatment.