Aim. To study the role of biomarkers in assessing the vulnerability of atherosclerotic plaques.Material and methods. A review of literature sources investigating the biomarker assessment of the vulnerability of atherosclerotic plaques published for the period 01.01.2016 to 31.12.2022 was carried out. Literature search was carried out in English and Russian in PubMed databases, in Google Academy, Elibrary.ru according to the following keywords: “biomarkers of plaque vulnerability”, “NLR and vulnerable plaque”, “CRP and vulnerable plaque”, ”MMP-9 and vulnerable plaque”, “TIMP-1 and vulnerable plaque”, ”galectin-3 and vulnerable plaque”, “NGAL and vulnerable plaque”. A total of 183 articles were found, of which 42 articles in full-text format containing original clinical studies were selected for the preparation of this review.Results. Numerous studies have shown that the vulnerability and rupture of the plaque, rather than its size and severity of stenosis, are the main cause of cardiovascular events in patients with coronary heart disease. Small plaques rich in lipids often become unstable due to an inflammatory reaction supported by the interaction between lipoproteins, monocytes, macrophages, T-lymphocytes and vascular wall cells. NLR, CRP, NGAL, Galectin-3, as well as markers of extracellular matrix degradation (MMP-9, TIMP-1) can play a special role in assessing the vulnerability of plaques.Conclusion. The development of acute coronary syndrome is based on the destabilization of the atherosclerotic plaque, which occurs not only due to changes in its lipid composition, but also infiltration by immuno-inflammatory cells, degradation of the extracellular matrix, as well as an active inflammatory reaction and neovascularization of the plaque. Therefore, traditional imaging methods that characterize the plaque by its appearance and size are not enough to predict the risk of rupture and the development of an acute thrombotic event. Thus, there is a need to identify new biomarkers that would correlate with the instability of plaque atheroma.