p38MAPK在慢性低氧性肺动脉高压中的作用研究进展  

Research advance of p38MAPK in chronic hypoxia-induced pulmonary hypertension

作　　者：韩小花[1] 程振玲[1] 施熠炜[2] 杜永成[1] 

机构地区：[1]山西医科大学附属人民医院呼吸科,太原030001 [2]山西医科大学第一医院呼吸科,太原030001

出　　处：《国际呼吸杂志》2013年第11期865-867,共3页International Journal of Respiration

摘　　要：肺动脉高压（PH）是一种具有潜在致命性的慢性肺循环疾病，临床表现为右心室后负荷增加，活动耐力下降，严重者可发生循环衰竭而死亡。其病因复杂，可由多种心、肺疾病或肺血管病引起，慢性低氧是PH的一个常见原因。慢性低氧可诱导p38MAPK激活，p38MAPK激活后能增加血管内皮生长因子的表达，血管内皮生长因子能够促进血管内皮细胞迁徙、增殖，从而导致PH的发生。因此，从p38MAPK信号通道角度研究是研究慢性低氧性肺动脉高压发生机制的新方向。Pulmonary hypertension （PH） is a potentially fatal chronic pulmonary disease, the clinical manifestation is right ventricular afterload increased, the activity endurance drop, the severer will circulatory failure and death. Its etiology complex, may be made of a variety of heart,lung diseases or pulmonary vascular diseases, chronic hypoxie is a common cause of PH. Chronic hypoxia can induce p38MAPK activate, activated p38MAPK can increase expressions of vascular endothelial growth factor （VEGF）, VEGF can promote vascular endothelial ceils migration, proliferation, thus leading to PH. Therefore, p38MAPK signaling pathway is the new direction of the pathogenesis of chronic hypoxic PH.

关 键 词：P38MAPK 慢性 低氧性肺动脉高压 

分 类 号：R544.16[医药卫生—心血管疾病]