CX3CL1-Fc treatment prevents atherosclerosis in Ldlr KO mice复制标题

CX3CL1-Fc治疗预防Ldlr KO小鼠动脉粥样硬化

The development of atherosclerotic plaques involves enhanced LDL trapping in the intima and formation of oxidized LDL, which leads to a series of processes including adhesion of monocytes to the endothelium, macrophage infiltration, cytokine release, and foam cell formation. Thus, macrophage accumulation during atherosclerosis progression contributes to inflammatory gene expression, foam cell accumulation, smooth muscle cell modulation, and endothelial wall thickening. Recruitment of monocytes to the endothelium is a key step in the development of atherosclerosis, and targeting this step can inhibit lesion formation. Two primary monocyte subsets exist in mice, classical Lys6ChiCX3CR1lo and patrolling Lys6CloCX3CR1hi cells.Both monocyte subsets are recruited to atherosclerotic vessels, but the majority are Lys6Chi. Once in the inflamed vessel, these monocytes can differentiate to M1-like macrophages that take up lipid and become foam cells. Endothelial cells also play a critical role in atherosclerosis, whereby pro-inflammatory conditions (e.g. high fat/high cholesterol diet) promote leukocyte adhesion.

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