Vol 14, No 4 (2023)

BACKGROUND: The study focused on the identification of new genetic predictors in the Russian population, particularly associations of the rs1132896 polymorphism of the matrix metalloproteinase type 2 gene (MMP-2) with the development of acute cerebrovascular accident (ACVA).

OBJECTIVE: To investigate the relationship of rs1132896 gene MMP-2 polymorphisms with ACVA development.

MATERIALS AND METHODS: The prospective, case–control study enrolled 318 patients with stroke (main group) and 323 controls (control group). The age of the patients in the main group ranged from 32 to 69 [57.0; 51.0–62.0] years. In the control group, the age of the patients ranged from 37 to 68 [55.0; 51.0–62.0] years, which was comparable to that of the main group. Sexual dimorphism was as follows: 191 men (age [56.5; 51.0–62.0]) and 127 women (age [57.0; 51.0–62.0]). The sex composition in the control group corresponded to that in the main group: 214 men (age [55.0; 51.0–62.0]) and 109 women (age [55.0; 51.0–62.0]). The main group underwent clinical examination, computed tomography of the brain, electrocardiography, echocardioscopy, duplex ultrasound scanning of the extracranial brachiocephalic arteries, 24-h monitoring of blood pressure and heart rate, and analysis of the blood coagulation system. Molecular genetic research was conducted at a branch of the Institute of Cytology and Genetics of the Siberian Branch of RAS (Novosibirsk). All patients provided written informed consent to participate voluntarily in the study. The duration of the study was 3 years, starting in 2019. The primary study endpoint was a diagnosis of stroke, verification of concomitant cardiovascular pathology, and risk factors for stroke development. Statistical processing of the results was performed using SPSS Statistics v. 22 (IBM Corp., USA) and MedCalc 22.006 (Microsoft, USA). When comparing extended variables, the Mann–Whitney U-test was used. Discrete values were compared using Pearson’s χ² test.

RESULTS: When analyzing statistical significance, a predominance of the homozygous CC genotype was recorded in the group of male patients with stroke: n=24 (12.6%) vs n=20 (9.3%; p=0.0324). In addition, in the group of women, a statistically significant predominance of the heterozygous CG genotype was noted in women with stroke: n=67 (52.8%) vs n=42 (38.5%; p=0.0420).

CONCLUSION: The homozygous CC genotype in men and the heterozygous CG genotype in women may be genetic predictors of the development of ACVA. The study of genetic factors in the development of ACVA is necessary to create a personalized approach to patient management at the outpatient and inpatient stages of medical care.

BACKGROUND: Among chronic noncommunicable diseases, cardiovascular diseases, particularly coronary heart disease (CHD), are the leading cause of death. The rennin-angiotensin-aldosterone system plays an important role in CHD development and progression; however, its role in the regulation of immunoneuroendocrine interactions requires further analysis.

OBJECTIVE: To study the relationship between angiotensin II (AT II) and molecular regulators of the activity of whole blood mononuclear cells (MNCs) in patients with angina pectoris.

MATERIALS AND METHODS: This cross-sectional study enrolled 65 patients with exertional angina aged 45–67 years, including 19 apparently healthy individuals. The levels of interleukins (ILs), transforming growth factor-β₁ (TGF-β₁), prostaglandin E₂ (PG E₂), serotonin, thyroid-stimulating hormone (TSH), and AT II in the blood serum were determined. In MNCs, the concentrations of protein kinases FAK, JNK, p38, and ERK, signal transducers, and activators of transcription (STAT 3, 5A, and 6) were determined.

RESULTS: In patients with coronary artery disease, the production of TGF-β₁ increased by 7.2% (p=0.00001), AT II by 136.9% (p=0.0001), serotonin by 129.0% (p=0.00001), IL-18 by 92.5% (p=0.00001), TSH by 51.7% (p=0.0012), ERK protein kinase content by 86.4% (p=0.0001), JNK by 56.8% (p=0.0001), and FAK by 55.3% (p=0.00002). The levels of IL-15 also decreased by 38.1% (p=0.0001), PG E₂ by 39.5% (p=0.0001), and STAT3 by 52.5% (p=0.0001).

CONCLUSION: The nature of the identified relationships among the analyzed factors allows us to consider AT II as a factor that ensures adaptive coupling of immune and neuroendocrine regulatory mechanisms in patients with coronary artery disease, contributing to a change in the balance between macrophages and T-helper types 1 and 2.

Despite significant advances in medicine, cardiovascular disease continues to be the leading cause of death worldwide. An important task in cardiology is the search and study of new cardiovascular biological markers. In recent years, salusins have attracted the interest of scientists. Salusins are endogenous biologically active peptides, which were first identified in 2003. Thus far, studies have demonstrated that salusin-α and salusin-β play important roles in vascular remodeling, inflammation, hypertension, and atherosclerotic processes. Salusin-α exhibits an antiatherogenic effect, whereas salusin-β plays a proatherogenic role. Despite the diverse biological, physiological, and pathophysiological aspects of salusins, the exact mechanism of their cardiovascular effects is not fully known. Further in-depth studies of the role of salusins in cardiovascular diseases are required. The regulation of the concentration and expression of salusin-α and salusin-β may prove to be a promising strategy for the treatment of patients with cardiac diseases.

Cardiovascular pathology is a leading cause of morbidity and mortality. An important task of modern cardiology is the search and study of new biological markers. Scientists’ interest is actively focused on the study of interleukin-38. Interleukin-38 is an anti-inflammatory cytokine and a member of the interleukin-1 family. This study aimed to analyze literature sources devoted to the study of interleukin-38 as a cardiovascular biological marker. Literature sources, including all relevant publications in PubMed (MEDLINE), RSCI, Google Scholar, and Science Direct, were analyzed. The search depth was 9 years. Interleukin-38 is found in the skin, heart, placenta, fetal liver, spleen, thymus, and activated B cells of the tonsils. Interleukin-38 protein is detected in human plasma, serum, and cell cultures by enzyme-linked immunosorbent assay. Interleukin-38 regulates immune and inflammatory responses by binding to its receptors and activating downstream signals. Its deficiency is associated with increased systemic inflammation in aging, cardiovascular diseases, and metabolic diseases. Currently, not much clinical and experimental data have been accumulated regarding the effect of interleukin-38 on the cardiovascular system; however, further studies are expected to demonstrate the possibility of its use as an additional laboratory tool for diagnosis and assessment of prognosis in patients with cardiac problems. Regulating the concentration and expression of interleukin-38 is a promising strategy for the treatment of cardiovascular diseases.