### Li et al uncover an unexpected effect of protein kinase C deletion on atherosclerosis. Excess lipids in the blood can activate monocytes and enhance their uptake into artery walls, thus promoting the development of atherosclerotic plaques. This lipid-induced activation of monocytes involves the signal transduction factor protein kinase C (PKC); but PKC has a number of isoforms, so exactly which enzyme is involved in the process, and how, remains unclear. To find out, Li and colleagues examined rats with hyperlipidemia. They showed that PKC levels were indeed increased in the animals’ monocytes, and that most of this was accounted for by an increase in PKCδ. To determine the physiological significance of this increase, the team generated transgenic atherosclerosis-prone mice with macrophages lacking PKCδ. To their surprise, …

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在这个问题上

Li等人揭示了蛋白激酶C缺失对动脉粥样硬化的意外影响。血液中过多的脂质会激活单核细胞并增强其对动脉壁的摄取，从而促进动脉粥样硬化斑块的形成。脂质诱导的单核细胞激活涉及信号转导因子蛋白激酶C（PKC）；但PKC具有许多同工型，因此尚不清楚该过程中涉及哪种酶以及如何参与。为了找出答案，李和同事检查了高脂血症大鼠。他们表明，动物单核细胞中的PKC水平确实增加了，而这大部分是由PKCδ的增加引起的。为了确定这种增加的生理学意义，研究小组用巨噬细胞缺乏PKCδ的方式转基因了易患动脉粥样硬化的小鼠。令他们惊讶的是……