药学前沿大讲堂第56讲-Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
报告题目：Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
讲座时间：
讲座地点：中山大学东校区bm11222宝马娱乐网站讲学厅（药学大楼125室）
主 讲 人：Professor Peter J. Little
主 持 人：黄民 教授、院长 郑文华 教授
bm11222宝马娱乐网站
Peter Little 教授简介：
Peter Little 教授于1979年在悉尼大学获博士学位，现为澳大利亚Baker IDI心脏与糖尿病研究所糖尿病和细胞生物学实验室主任，澳洲生物脉管学会会长，Monash University及RMIT University荣誉教授，peter教授长期致力于细胞信号转导及药物研究等方面的工作。近年来，peter教授先后在J Cell Mol Medicine， Curr. Opinion Lipidology ，Endocrine Reviews ，Arterioscler. Throm. Vasc. Biol，J. Biol. Chem.等世界著名杂志发表了多篇文章。
摘要:
Atherosclerosis commences with the binding of Low Density Lipoproteins (LDL) to modified proteoglycans. Modifications to proteoglycans which make the environment “stickier” for LDL arise from the actions of growth factors in the vessel wall. The signaling pathways therefore represent therapeutic targets for the prevention of atherosclerosis. We discovered that the protein tyrosine kinase (PTK) inhibitor, imatinib , inhibits proteoglycan synthesis and modifies the structure in a manner that reduces binding of proteoglycans to LDL and reduces the deposition of lipid in the vessel wall of high fat fed atherosclerosis-prone mice. Imatinib inhibits multiple PTK including the Platelet-derived growth factor (PDGF) receptor. The PTKs which are inhibited by imatinib represent targets for the prevention of atherosclerosis.
