Li Chi-Yuan, Lin Feng-Yen
Acta Anaesthesiol Taiwan. 2007 Jun;45(2):63-4.
The p47phox- and Rac 1-dependent NADPH oxidase activation, ROS production, and MAPK signaling pathways play critical roles in endotoxin-enhanced TLR4 expression and TLR4 mRNA stabilization in VSMCs. These evidences provide for the direct involvement of VSMCs in endotoxin-mediated inflammatory activation, which may contribute to the progression of cardiovascular disorders, although targeting TLR4 will prove to be a successful approach for the treatment of these devastating diseases remains to be determined.
p47phox和Rac 1依赖性NADPH氧化酶激活、活性氧生成以及丝裂原活化蛋白激酶（MAPK）信号通路在内毒素增强血管平滑肌细胞（VSMCs）中Toll样受体4（TLR4）表达和TLR4 mRNA稳定性方面发挥关键作用。这些证据表明VSMCs直接参与内毒素介导的炎症激活，这可能促进心血管疾病的进展，尽管靶向TLR4是否会被证明是治疗这些严重疾病的成功方法仍有待确定。
