{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T12:44:54Z","timestamp":1790685894818,"version":"4.1.0"},"reference-count":32,"publisher":"ALUNA","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Wiad Lek"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:p>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\u00acplications. 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-1\u03b2, IL-6, TNF-\u03b1 (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.<\/jats:p>","DOI":"10.36740\/wlek202211224","type":"journal-article","created":{"date-parts":[[2023,1,1]],"date-time":"2023-01-01T21:20:11Z","timestamp":1672608011000},"page":"2862-2866","source":"Crossref","is-referenced-by-count":36,"title":["HOMOCYSTEINE AND CARDIOVASCULAR DISEASE \u2013 A CURRENT REVIEW"],"prefix":"10.36740","volume":"75","author":[{"given":"Alicja","family":"Gospodarczyk","sequence":"first","affiliation":[{"name":"DEPARTMENT OF BIOCHEMISTRY, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kamil","family":"Marczewski","sequence":"additional","affiliation":[{"name":"DEPARTMENT OF EMERGENCY MEDICINE, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalia","family":"Gospodarczyk","sequence":"additional","affiliation":[{"name":"DEPARTMENT OF EMERGENCY MEDICINE, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Micha\u0142","family":"Widuch","sequence":"additional","affiliation":[{"name":"DEPARTMENT OF BIOCHEMISTRY, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Micha\u0142","family":"Tkocz","sequence":"additional","affiliation":[{"name":"UROLOGICAL DEPARTMENT OF MUNICIPAL HOSPITAL, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jolanta","family":"Zalejska-Fiolka","sequence":"additional","affiliation":[{"name":"DEPARTMENT OF BIOCHEMISTRY, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"22436","published-online":{"date-parts":[[2022]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1. \u0160kovierov\u00e1 H, Vidomanov\u00e1 E, Mahmood S et al. 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