APELIN IN HEART FAILURE.

Apelin is a biologically active protein encoded by the APLN gene. It was first isolated in 1998 as a ligand for the APJ receptor. It exists in several isoforms differing in polypeptide chain length and biological activity. It is secreted by white adipose tissue, and its expression has been identified in many body tissues, including the cardiovascular system, kidneys, lungs, CNS (especially the hypothalamus, suprachiasmatic and ventricular nuclei), skeletal muscle, mammary glands, adrenal glands, ovaries, stomach, liver cells, placenta, and breast milk. However, the highest concentrations were observed in the endocardium and endothelium of vascular smooth muscle cells. In myocardial tissue, apelin has a positive inotropic effect and exerts an opposing effect to the RAA (renin-angiotensin-aldosterone) system, lowering blood pressure. Therefore, its positive role in early stages of heart failure, in patients with hypertension and ischemic heart disease is emphasized. The synthesis and secretion of apelin by adipocytes makes it possible to classify this peptide as an adipokine. Therefore, its production in adipose tissue is enhanced in obesity. Furthermore, apelin has been shown to increase cellular sensitivity to insulin and improve glucose tolerance in the onset of type 2 diabetes, and therefore appears to play a significant role in the pathogenesis of metabolic disease. An accurate assessment of the importance of apelin in cardiovascular disease requires further studies, which may contribute to the use of apelin in the treatment of heart failure.

HOMOCYSTEINE AND CARDIOVASCULAR DISEASE - A CURRENT REVIEW.

Cardiovascular diseases remain the leading cause of death worldwide for the past 20 years. Of these, ischemic heart disease has the highest mortality rate. In over 98% of cases it is caused by atherosclerosis of the coronary arteries. Homocysteine is an amino acid, containing a sulfhydryl group, which is formed as a result of the metabolism of the amino acids methionine and cysteine, which is supplied with protein-containing foods. A small amount of it is necessary for the proper functioning of the body, however, an increased concentration in blood plasma, which hyperhomocysteinemia, negatively affects blood vessels leading to the development of atherosclerosis and thrombotic com¬plications. The adverse effect on blood vessels results from various mechanisms, such as: excessive activation of Toll-like 4 receptor, activation N-methyl-d-aspartate receptors, increased production of reactive oxygen species, and impairment of nitric oxide synthesis. Elevated levels of reactive oxygen species are associated with increased expression of proinflammatory cytokines such as IL-1ß, IL-6, TNF-α (tumor necrosis tumor necrosis factor), MCP-1 and intracellular adhesion molecule-1. Another factor contributing to hyperhomocysteinemia is mutation of the MTHFR gene, which in normal conditions is responsible for maintaining homocysteine levels within the normal range. People with MTHFR mutation are more prone to develop atherosclerosis and the following complications: myocardial infarction, stroke, thrombotic episodes and coronary artery disease. The aim of this paper is to present evidence supporting the role of homocysteine in the development of many cardiovascular diseases.