Glial cell dysfunction in the pathogenesis of heart failure

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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.