丝裂原活化蛋白激酶在动脉粥样硬化中作用的相关性研究

动脉粥样硬化(AS)是动脉的慢性炎性疾病。AS由炎症引发血管内皮细胞活化,包括释放细胞因子,粘附分子,基质金属蛋白酶和其它调节炎性介质(包括NO),导致血管内皮细胞功能紊乱和损伤,这是早期AS泡沫细胞形成的关键因素之一。丝裂原活化蛋白激酶(MAPKs)是调控炎症和抗炎反应重要的信号通路。激活的MAPKs,特别是ERK、JNK和p38 MAPKs,参与调节粘附分子和基质金属蛋白酶的表达。靶向给予ERK,JNK和p38 MAPKs信号通路抑制剂,其临床前研究数据表明它们有抗炎活性。因此,MAPKs的特异性抑制剂有望成为一种新的减轻动脉粥样化形成的治疗方法。

The relevant research on the role of Mitogen-activated protein kinases in atheroselerosis

Atherosclerosis is a chronic inflammatory disease of arteries. It is initiated by excessive inflammation stimulates the endothelial cells activation, including secrete cytokines, adhesion molecules, matrix metalloproteinases and other inflammatory mediators, including nitric oxide. This may lead to endothelial cells dysfunction and injury, and it is a key factor for foamcellSformation, an early stage of atherosclerosis. Mitogen-activated protein kinases (MAPKs) are regarded as critical signal pathway mediating inflammation and anti-inflamamation.Multiple researchs indicate that increased activity of MAPKs,in particular ERK,JNK and p38 MAPK,regulating expression of adhesion molecules and matrix metalloproteinases. Inhibitors targeting ERK,JNK and p38 MAPK pathways have been developed, and preclinical datas suggest that they exhibit anti-inflammatory activity. Thus, specific inhibition of MAPKs activity may emerge as a novel and promising therapeutic approach to attenuate atheroma formation in the future.