心力衰竭中枢机制的研究进展及治疗展望
详细信息    查看全文 | 推荐本文 |
  • 英文篇名:Advances in Research on Central Mechanism of Heart Failure and Outlook of Therapy
  • 作者:吴帆 ; 刘地川
  • 英文作者:WU Fanyu;LIU Dichuan;Chongqing Medical University Graduate School;Cardiovascular Internal Medicine,The Second Affiliated Hospital of Chongqing Medical University;
  • 关键词:心力衰竭 ; 下丘脑室旁核 ; 炎性细胞因子 ; 肾素-血管紧张素-醛固酮系统
  • 英文关键词:Heart failure;;Periventricular nucleus;;Proinflammatory cytokines;;Renin-angiotensin-aldosterone system
  • 中文刊名:XXGB
  • 英文刊名:Advances in Cardiovascular Diseases
  • 机构:重庆医科大学研究生院;重庆医科大学附属第二医院心血管内科;
  • 出版日期:2019-01-25 10:05
  • 出版单位:心血管病学进展
  • 年:2019
  • 期:v.40;No.209
  • 基金:国家自然科学基金面上项目(30670870);; 重庆市科委项目(CSTC2012jjA10085)
  • 语种:中文;
  • 页:XXGB201901016
  • 页数:4
  • CN:01
  • ISSN:51-1187/R
  • 分类号:63-66
摘要
心血管疾病已成为严重危害生命健康的主要疾病之一,目前受到人们越来越多的关注。心力衰竭是心内科常见疾病之一,尽管目前对于心力衰竭的治疗已有较为丰富的经验,但它仍有着较高的死亡率,因此人们不断探寻新的治疗靶点,而心力衰竭中枢机制的干预就是一个潜在的治疗靶点。越来越多的证据表明下丘脑室旁核内的炎性细胞因子及肾素-血管紧张素系统等在心力衰竭的发生发展过程中起着单独或协同的作用。
        Cardiovascular disease has been recognized as a major disease to do harm to life health,and it is getting more and more attention. Heart failure( HF) is a common disease in Department of Cardiology,although we have extensive experience in treating HF,it still remains high mortality rate. Thus,researches persistently explore the new treatment targets,among those,the intervention of central mechanism of HF is a potential treatment target. More and more researches show that proinflammatory cytokines,renin-angiotensin system and so on in periventricular nucleus may develop HF alone or synergistically.
引文
[1]Roger VL,Go AS,Lloyd-Jones DM,et al.Heart disease and stroke statistics-2012 update:a report from the American Heart Association[J].Circulation,2012,125(1):e2-e220.
    [2]Chen F,Liu F,Badoer E.AT1 receptors in the paraventricular nucleus mediate the hyperthermia-induced reflex reduction of renal blood flow in rats[J].Am JPhysiol Regul Integr Comp Physiol,2011,300(2):R479-485.
    [3]Isegawa K,Hirooka Y,Katsuki M,et al.AngiotensinⅡtype 1 receptor expression in astrocytes is upregulated leading to increased mortality in mice with myocardial infarction-induced heart failure[J].Am J Physiol Heart Circ Physiol,2014,307(10):H1448-1455.
    [4]Ren X,Zhang F,Zhao M,et al.Angiotensin-(1-7)in paraventricular nucleus contributes to the enhanced cardiac sympathetic afferent reflex and sympathetic activity in chronic heart failure rats[J].Cell Physiol Biochem,2017,42(6):2523-2539.
    [5]Zhong MK,Duan YC,Chen AD,et al.Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats[J].Exp Physiol,2008,93(6):746-753.
    [6]Zhang ZH,Yu Y,Kang YM,et al.Aldosterone acts centrally to increase brain renin-angiotensin system activity and oxidative stress in normal rats[J].Am JPhysiol Heart Circ Physiol,2008,294(2):H1067-1074.
    [7]Gao L,Wang WZ,Wang W,et al.Imbalance of angiotensin type 1 receptor and angiotensinⅡtype 2 receptor in the rostral ventrolateral medulla:potential mechanism for sympathetic overactivity in heart failure[J].Hypertension,2008,52(4):708-714.
    [8]Zheng H,Li YF,Wang W,et al.Enhanced angiotensin-mediated excitation of renal sympathetic nerve activity within the paraventricular nucleus of anesthetized rats with heart failure[J].Am J Physiol Regul Integr Comp Physiol,2009,297(5):R1364-1374.
    [9]Zera T,Ufnal M,Szczepanska-Sadowska E.TNF and angiotensin type 1 receptors interact in the brain control of blood pressure in heart failure[J].Cytokine,2015,71(2):272-277.
    [10]Dupont AG,Brouwers S.Brain angiotensin peptides regulate sympathetic tone and blood pressure[J].J Hypertens,2010,28(8):1599-1610.
    [11]Lu N,Helwig BG,Fels RJ,et al.Central Tempol alters basal sympathetic nerve discharge and attenuates sympathetic excitation to central AngⅡ[J].Am JPhysiol Heart Circ Physiol,2004,287(6):H2626-2633.
    [12]Francis J,Weiss RM,Wei SG,et al.Central mineralocorticoid receptor blockade improves volume regulation and reduces sympathetic drive in heart failure[J].Am J Physiol Heart Circ Physiol,2001,281(5):H2241-2251.
    [13]Kang YM,Zhang AQ,Zhao XF,et al.Paraventricular nucleus corticotrophin releasing hormone contributes to sympathoexcitation via interaction with neurotransmitters in heart failure[J].Basic Res Cardiol,2011,106(3):473-483.
    [14]Francis J,Weiss RM,Johnson AK,et al.Central mineralocorticoid receptor blockade decreases plasma TNF-alpha after coronary artery ligation in rats[J].Am J Physiol Regul Integr Comp Physiol,2003,284(2):R328-335.
    [15]Bradham WS,Moe G,Wendt KA,et al.TNF-alpha and myocardial matrix metalloproteinases in heart failure:relationship to LV remodeling[J].Am J Physiol Heart Circ Physiol,2002,282(4):H1288-1295.
    [16]Kang YM,Zhang ZH,Xue B,et al.Inhibition of brain proinflammatory cytokine synthesis reduces hypothalamic excitation in rats with ischemia-induced heart failure[J].Am J Physiol Heart Circ Physiol,2008,295(1):H227-236.
    [17]Mariappan N,Soorappan RN,Haque M,et al.TNF-alpha-induced mitochondrial oxidative stress and cardiac dysfunction:restoration by superoxide dismutase mimetic Tempol[J].Am J Physiol Heart Circ Physiol,2007,293(5):H2726-2737.
    [18]Kang YM,Wang Y,Yang LM,et al.TNF-alpha in hypothalamic paraventricular nucleus contributes to sympathoexcitation in heart failure by modulating AT1 receptor and neurotransmitters[J].Tohoku J Exp Med,2010,222(4):251-263.
    [19]Tsutsui H,Kinugawa S,Matsushima S.Oxidative stress and heart failure[J].Am J Physiol Heart Circ Physiol,2011,301(6):H2181-2190.
    [20]Lindley TE,Doobay MF,Sharma RV,et al.Superoxide is involved in the central nervous system activation and sympathoexcitation of myocardial infarction-induced heart failure[J].Circ Res,2004,94(3):402-409.
    [21]Han Y,Shi Z,Zhang F,et al.Reactive oxygen species in the paraventricular nucleus mediate the cardiac sympathetic afferent reflex in chronic heart failure rats[J].Eur J Heart Fail,2007,9(10):967-973.
    [22]Kang YM,Gao F,Li HH,et al.NF-kappaB in the paraventricular nucleus modulates neurotransmitters and contributes to sympathoexcitation in heart failure[J].Basic Res Cardiol,2011,106(6):1087-1097.
    [23]Kang YM,Yang Q,Yu XJ,et al.Hypothalamic paraventricular nucleus activation contributes to neurohumoral excitation in rats with heart failure[J].Regen Med Res,2014,2(1):2.
    [24]Liu Q,Wang T,Yu H,et al.Interaction between interleukin-1 beta and angiotensinⅡreceptor 1 in hypothalamic paraventricular nucleus contributes to progression of heart failure[J].J Interferon Cytokine Res,2014,34(11):870-875.
    [25]Wang T,Gao W,Xiao K,et al.Interaction between interleukin 6 and angiotensinⅡreceptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure[J].Mol Med Rep,2017,15(6):4259-4265.
    [26]Zera T,Ufnal M,Szczepanska-Sadowska E.Central TNF-alpha elevates blood pressure and sensitizes to central pressor action of angiotensinⅡin the infarcted rats[J].J Physiol Pharmacol,2008,59(Suppl 8):117-121.
    [27]Kang YM,Ma Y,Elks C,et al.Cross-talk between cytokines and renin-angiotensin in hypothalamic paraventricular nucleus in heart failure:role of nuclear factor-kappaB[J].Cardiovasc Res,2008,79(4):671-678.
    [28]Yu XJ,Suo YP,Qi J,et al.Interaction between AT1 receptor and NF-kappaBin hypothalamic paraventricular nucleus contributes to oxidative stress and sympathoexcitation by modulating neurotransmitters in heart failure[J].Cardiovasc Toxicol,2013,13(4):381-390.
    [29]Zhang WW,Bai F,Wang J,et al.Edaravone inhibits pressure overload-induced cardiac fibrosis and dysfunction by reducing expression of angiotensinⅡAT1 receptor[J].Drug Des Devel Ther,2017,10(11):3019-3033.
    [30]Zhang Y,Yang Y,Zhang GZ,et al.Stereotactic administration of edaravone ameliorates collagenase-induced intracerebral hemorrhage in rat[J].CNS Neurosci Ther,2016,22(10):824-835.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700