Glial cell dysfunction in the pathogenesis of heart failure

我们已经证明，在慢性心力衰竭的发病机制中，脑干心血管中心的氧化应激有助于交感神经亢进。在本研究中，我们有新的发现，在心力衰竭模型大鼠脑干心血管中心，由小胶质细胞toll样受体4介导的炎症级联激活通过星形胶质细胞凋亡引起交感神经过度活跃，而星形胶质细胞对神经元有保护作用。

We have demonstrated that oxidative stress in the cardiovascular center of the brainstem contributes to the sympathetic hyperactivity in the pathogenesis of chronic heart failure. In the present study, we have novel new findings, following that the activation of inflammatory cascade mediated by toll-like receptor 4 in the microglia causes sympathetic hyperactivity via apoptosis of astrocyte, which has a protective effect for neuron, in the cardiovascular center of the brainstem of heart failure model rats.