Regulatory effects of statins on CCL2/CCR2 axis in cardiovascular diseases: new insight into pleiotropic effects of statins

• Published in: Journal of inflammation (London, England) England), 2024-12, Vol.21 (1), p.51-19, Article 51
• Main Authors: Gholamalizadeh, Hanieh, Ensan, Behzad, Karav, Sercan, Jamialahmadi, Tannaz, Sahebkar, Amirhossein
• Format: Article
• Language: English
• Subjects: Analysis; Atherosclerosis; Cardiovascular agents; CCL2; Heart diseases; Inflammation; Ischemic heart disease; Macrophages; MCP-1; Statins; Stroke; Stroke (Disease)
• ISSN: 1476-9255; 1476-9255
• DOI: 10.1186/s12950-024-00420-y

HMG-CoA reductase inhibitors are well-known medications in the treatment of cardiovascular disorders due to their pleiotropic and lipid-lowering properties. Herein, we reviewed the effects of statins on the CCL2/CCR2 axis. Scopus and Pubmed databases were systematically searched using the following keywords:" Hydroxymethylglutaryl CoA Reductase Inhibitors"," HMG-CoA Reductase Inhibitors"," Statins", "CCL2, Chemokine", "Monocyte Chemoattractant Protein-1" and "Chemokine (C-C Motif) Ligand 2". Evidence investigating the role of statin on MCP-1 in CVD was identified and bibliographies were completely evaluated to gather further related studies. The anti-inflammatory effects of statins on the CCL2/CCR2 pathway have been widely investigated. Despite inconclusive results, a great body of research supports the regulatory roles of statins on this pathway due to their pleiotropic effects. By disrupting the CCL2/CCR2 axis, statins attenuate the infiltration of monocytes and macrophages into the zone of inflammation and hence down-regulate the inflammatory cascades in various CVDs including atherosclerosis, cardiac remodeling, and stroke, among others. CCL2 plays a major role in the pathogenesis of cardiovascular disorders. Down-regulation of CCL2 is proposed as one of the pleiotropic properties of statins. However, more investigations are required to elucidate which statin in what dose exerts a more potent effect on CCL2/CCR2 pathway.