 The study investigates the anti-Atherosclerotic effects of Helix B surface peptid, HBSP, and non-Erythropoietin, tissue-protective compound derived from EPO, in human umbilical vein endothelial cells, HUVCs, and human monocytic THP, one cells in vitro and what an abe heritable hyperlipidemic spontaneous myocardial infarction, WHHLMI, rabbits in vivo. HBSP inhibited apoptosis induced by seriactive protein, CRP, a direct mediator of atherosclerosis, through activation of act. HBSP also attenuated CRP-induced production of tumor necrosis factor, TNF, alpha and matrix metalloprotonase 9 in THP1 cells. In the WHHLMI rabbit, HBSP significantly suppressed progression of coronary atherosclerotic lesions as assessed by mean cross-sectional stenosis and inhibited coronary artery endothelial cell apoptosis with increased activation of act. Furthermore, TNF expression and the number of M1 macrophages and M1, M2 macrophage ratio in coronary atherosclerotic lesions were markedly reduced in HBSP treated animals. The study demonstrates that HBSP suppresses coronary atherosclerosis, in part by inhibiting endothelial cell apoptosis through activation of act and in association with decreased TNF production and modified macrophage polarization in coronary atherosclerotic lesions. Because HBSP does not have the prothrombotic effects of EPO, the study may provide a novel therapeutic strategy that prevents progression of coronary artery disease. This article was authored by Hiroto Yuba, Masashi Shiyomi, Michael Brines, and others. We are article.tv, links in the description below.