Muslin Anthony J
Center for Cardiovascular Research, John Milliken Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA.
Clin Sci (Lond). 2008 Oct;115(7):203-18. doi: 10.1042/CS20070430.
Intracellular MAPK (mitogen-activated protein kinase) signalling cascades probably play an important role in the pathogenesis of cardiac and vascular disease. A substantial amount of basic science research has defined many of the details of MAPK pathway organization and activation, but the role of individual signalling proteins in the pathogenesis of various cardiovascular diseases is still being elucidated. In the present review, the role of the MAPKs ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPK in cardiac hypertrophy, cardiac remodelling after myocardial infarction, atherosclerosis and vascular restenosis will be examined, with attention paid to genetically modified murine model systems and to the use of pharmacological inhibitors of protein kinases. Despite the complexities of this field of research, attractive targets for pharmacological therapy are emerging.
细胞内丝裂原活化蛋白激酶(MAPK)信号级联反应可能在心脏和血管疾病的发病机制中起重要作用。大量基础科学研究已明确了MAPK信号通路组织和激活的许多细节,但单个信号蛋白在各种心血管疾病发病机制中的作用仍在阐明之中。在本综述中,将探讨MAPK家族成员细胞外信号调节激酶(ERK)、c-Jun氨基末端激酶(JNK)和p38 MAPK在心肌肥大、心肌梗死后心脏重塑、动脉粥样硬化和血管再狭窄中的作用,重点关注基因改造小鼠模型系统以及蛋白激酶药理学抑制剂的应用。尽管该研究领域存在复杂性,但药理学治疗的有吸引力靶点正在浮现。