Targeting the CXCR4/DEL-1 axis to tackle atherosclerosis.

Atherosclerosis is a chronic disease of the arteries whose fundamental lesion is atherosclerotic plaque [ [1] Pedicino D. Giglio A.F. Galiffa V.A. Cialdella P. Trotta F. Graziani F. Liuzzo G. Infections, immunity and atherosclerosis: pathogenic mechanisms and unsolved questions. Int. J. Cardiol. 2013; 166: 572-583https://doi.org/10.1016/j.ijcard.2012.05.098 Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar ]. In recent decades, researchers have focused their attention on plasma low-density lipoprotein cholesterol (LDL-C) levels, demonstrating their close correlation with the development of atherosclerosis [ [2] De Luca L. Arca M. Temporelli P.L. Meessen J. Riccio C. Bonomo P. Colavita A.R. Gabrielli D. Gulizia M.M. Colivicchi F. et al. Current lipid lowering treatment and attainment of LDL targets recommended by ESC/EAS guidelines in very high-risk patients with established atherosclerotic cardiovascular disease: insights from the START registry. Int. J. Cardiol. 2020; 316: 229-235https://doi.org/10.1016/j.ijcard.2020.05.055 Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar ]. In the early stages, endothelial dysfunction allows the accumulation of LDL particles within the walls of some of the more susceptible vascular segments. LDL particles will later change by undergoing oxidation (oxLDL). In parallel, inflammatory cells, especially monocytes/macrophages, are recruited to the intima of these vessels and, after absorbing oxLDL, form foam cells contributing to the onset and progression of the atherogenic process. DEL-1 suppression attenuates atherosclerosis by modulating macrophagic GSK-3β/CEBP-β signaling pathwayInternational Journal of CardiologyVol. 376PreviewThe study aims to investigate the effect of developmental endothelial locus-1(DEL-1) expression in atherosclerotic plaque formation and its mechanism. Full-Text PDF