细胞周期蛋白依赖性激酶9可能作为下调动脉粥样硬化炎症的新靶点（综述）。
Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review).
作者信息
Han Yeming, Zhan Yang, Hou Guihua, Li Li
机构信息
Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China.
Institute of Experimental Nuclear Medicine, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.
出版信息
Biomed Rep. 2014 Nov;2(6):775-779. doi: 10.3892/br.2014.322. Epub 2014 Jul 31.
Inflammation is a key component of atherosclerosis. Genes coding for inflammatory or anti-inflammatory molecules are considered good candidates for estimating the risk of developing atherosclerosis. Cyclin-dependent kinase 9 (CDK9), the kinase of positive transcription elongation factor b (P-TEFb), is crucial in the cell cycle and apoptosis. Previous studies have focused on its inhibition of immune cells for the resolution of inflammation. Considering the effects of inflammation in the pathogenicity of atherosclerosis, decreasing inflammation through the inhibition of CDK9 may be useful for the prognosis of atherosclerosis. The aim of this review was to examine whether inhibition of the CDK9 monocyte may affect the process of inflammation by acting on the cytokine secretion and interacting with endothelial cells (ECs). Thus, CDK9 may be a novel target for the diagnosis and therapy of atherosclerosis.
炎症是动脉粥样硬化的关键组成部分。编码炎症或抗炎分子的基因被认为是评估动脉粥样硬化发生风险的良好候选基因。细胞周期蛋白依赖性激酶9（CDK9），即正转录延伸因子b（P-TEFb）的激酶，在细胞周期和细胞凋亡中起关键作用。先前的研究集中在其对免疫细胞的抑制作用以解决炎症。考虑到炎症在动脉粥样硬化发病机制中的作用，通过抑制CDK9来减轻炎症可能对动脉粥样硬化的预后有益。本综述的目的是研究抑制CDK9单核细胞是否可能通过作用于细胞因子分泌并与内皮细胞（ECs）相互作用来影响炎症过程。因此，CDK9可能是动脉粥样硬化诊断和治疗的新靶点。
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