### The kinase LKB1 slows foam cell formation and atherosclerosis progression in mice, report Liu et al. Atherosclerosis begins with the gradual accumulation of fatty deposits on blood vessel walls. Monocytes are recruited to the lesions where they convert to macrophages to phagocytose lipids in the lesions. Continued lipid uptake by the macrophages transforms them into foam cells, which is a critical step in plaque development. However, mechanisms underlying this transformation remain unclear. Liu and colleagues now show that the kinase LKB1, previously identified as having cardioprotective and anti-inflammatory effects, is a negative regulator of foam cell development. They found that, in mice prone to atherosclerosis, the levels of LKB1 in plaque macrophages decreases with disease progression. This decrease prevented LKB1-directed phosphorylation of scavenger receptor A (SRA)—a …

中文翻译：

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在这个问题上

Liu等报道，LKB1激酶减慢了小鼠的泡沫细胞形成和动脉粥样硬化的进展。动脉粥样硬化始于脂肪沉积在血管壁上的逐渐积累。单核细胞被募集到病变处，在此它们转化为巨噬细胞以吞噬病变中的脂质。巨噬细胞对脂质的持续摄取将其转化为泡沫细胞，这是噬菌斑形成的关键步骤。但是，这种转变的机制尚不清楚。Liu和同事现在显示，以前被鉴定为具有心脏保护和抗炎作用的LKB1激酶是泡沫细胞发育的负调节剂。他们发现，在易患动脉粥样硬化的小鼠中，斑块巨噬细胞中LKB1的水平随疾病进展而降低。