©　2017,　Editorial　Board　of　Journal　of　Xi＇an　Jiaotong　University　(Medical　Sciences).　All　right　reserved.　Heart　failure　is　a　complex　clinical　syndrome,　and　impaired　filling　or　ejection　disorders　result　from　any　ventricular　structure　or　dysfunction　can　cause　heart　failure.　The　prevalence　of　heart　failure　in　adult　populations　in　developed　countries　has　reached　1%　to　2%,　while　the　prevalence　in　elderly　people　over　70　years　of　age　has　increased　to　≥10%.　With　the　population　aging　and　the　prevalence　of　coronary　heart　disease　increased,　the　prevalence　of　heart　failure　has　increased,　becoming　a　disable　and　fatal　disease.　The　changes　of　the　central　nervous　system　hormones　such　as　renin-angiotensin　system　(RAS),　inflammatory　cytokines　(proinflammatory　cytokines,　PIC),　and　reactive　oxygen　species　(ROS)　may　be　closely　related　to　increased　central　activity　in　heart　failure,　which　can　significantly　alter　the　activities　of　peripheral　sympathetic　nerves.　Constant　sympathetic　nervous　activity　is　an　important　cause　of　development　of　heart　failure,　so　reducing　the　sympathetic　excitability　of　heart　failure　is　regarded　as　one　of　the　focuses　of　treatment　and　research.　This　paper　focuses　on　the　influence　of　central　neurohormone　on　heart　failure　and　possible　central　mechanism.