Targeting inflammation in atherosclerosis: prospects and limitations

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Abstract

Despite the effective measures of hypolipidemic and hypotensive therapy, the management of metabolic disorders, and smoking control, many patients are still at risk of atherosclerosis and cardiovascular diseases remain the leading causes of mortality. In order to address this issue, efforts are being made to manage the residual risk of cardiovascular events, particularly by suppressing inflammation in the vascular wall. Anti-inflammatory therapies currently tested in clinical trials lead to a certain reduction in the risk of atherosclerosis and its clinical manifestations. However, some studies show that this therapy may also increase the risk of fatal infections. Moreover, suppressing inflammation in the vessel wall may slow down the removal of cholesterol, which could be considered a potential drawback of this treatment approach.

This review investigates the involvement of various inflammatory factors in the development of atherosclerosis, both at the early and late stages, provides clinical evidence on the association between inflammation and atherogenesis and the effect of anti-inflammatory therapies in preventing the development of atherosclerotic complications. Based on these findings, we analyze the potential prospects and limitations of anti-inflammatory medications in atherosclerosis treatment. The review also explores promising alternative approaches targeting the immune system as means of atherosclerosis management and prevention of its complications.

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About the authors

Dmitry A. Tanyanskiy

Institute of Experimental Medicine

Author for correspondence.
Email: dmitry.athero@gmail.com
ORCID iD: 0000-0002-5321-8834
SPIN-code: 9303-9445

MD, Dr. Sci. (Medicine), Assistant Professor

Russian Federation, Saint Petersburg

Alexander D. Denisenko

Institute of Experimental Medicine

Email: add@iem.spb.ru
ORCID iD: 0000-0003-1613-0654
SPIN-code: 7496-1449

MD, Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

Peter V. Pigarevsky

Institute of Experimental Medicine

Email: pigarevsky@mail.ru
ORCID iD: 0000-0002-5906-6771
SPIN-code: 8636-4271

Dr. Sci. (Biology)

Russian Federation, Saint Petersburg

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2. Fig. 1. The interplay of vascular cells during atherosclerosis: A, apoptotic bodies; AB, anti-lipoprotein antibodies; B, B cells; EC, endothelial cells; ECM, extracellular matrix; ICAM-1 and VCAM-1, intercellular and vascular adhesion molecules; IL, interleukin; IFN-γ, interferon-γ; FC, foam cells; HDL, high-density lipoproteins; L, lymphocytes; LDL, low-density lipoproteins; M1 and M2, M1 and M2 macrophages; mLDL, modified low-density lipoproteins; MMP, matrix metalloproteinases; Mono, monocyte; NC, necrotic core; PRR, pattern recognition receptor; SMC, smooth muscle cell; SR, scavenger receptor; NLRP3, NLR family pyrin domain-containing 3 inflammasome; T- thrombus; Th1 and Th2, type 1 and 2 T helper cells; TNF, tumor necrosis factor; TGF-β, transforming growth factor beta; Treg, regulatory T cells.

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