CardioSomaticsPub Date : 2023-12-20DOI: 10.17816/cs623020
A. M. Alieva, I. Baykova, T. Pinchuk, I. A. Kotikova, I. G. Nikitin
{"title":"Interleukin-38 and cardiovascular pathology: literature review","authors":"A. M. Alieva, I. Baykova, T. Pinchuk, I. A. Kotikova, I. G. Nikitin","doi":"10.17816/cs623020","DOIUrl":"https://doi.org/10.17816/cs623020","url":null,"abstract":"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.","PeriodicalId":502399,"journal":{"name":"CardioSomatics","volume":"32 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139168265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
CardioSomaticsPub Date : 2023-12-20DOI: 10.17816/cs492285
V. Parfenyuk, A. V. Logatkina, Stanislav S. Bondar, I. Terekhov, V. Nikiforov
{"title":"Role of angiotensin II and neuroendocrine factors in immunological regulation in patients with coronary heart disease: prospective cross-sectional study","authors":"V. Parfenyuk, A. V. Logatkina, Stanislav S. Bondar, I. Terekhov, V. Nikiforov","doi":"10.17816/cs492285","DOIUrl":"https://doi.org/10.17816/cs492285","url":null,"abstract":"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.","PeriodicalId":502399,"journal":{"name":"CardioSomatics","volume":"12 s1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139168035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}