[1]廖光芝 高电萨.病毒性心肌炎性别差异研究进展[J].心血管病学进展,2020,(2):144-147.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.011]
 LIAO Guangzhi,GAO Diansa.Gender Bias in Viral Myocarditis[J].Advances in Cardiovascular Diseases,2020,(2):144-147.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.011]
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病毒性心肌炎性别差异研究进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年2期
页码:
144-147
栏目:
综述
出版日期:
2020-02-25

文章信息/Info

Title:
Gender Bias in Viral Myocarditis
作者:
廖光芝1 高电萨2
重庆医科大学,重庆4000102.重庆医科大学附属第一医院心血管内科,重庆400010
Author(s):
LIAO Guangzhi1GAO Diansa2
(1.Chongqing Medical University,Chongqing 400010,China; 2.The First Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China)
关键词:
病毒性心肌炎性别差异性激素
Keywords:
Viral myocarditis Gender bias Sex hormone
DOI:
10.16806/j.cnki.issn.1004-3934.2020.02.011
摘要:
病毒性心肌炎是导致青少年猝死的常见原因之一。研究发现病毒性心肌炎在发病率和临床表现方面显示出较为明显的性别差异,相比男性而言,女性发病率低且病情轻,后期发展为扩张型心肌病甚至心力衰竭的概率低,预后佳。近年来研究者们从不同方面对产生这一性别差异的机制作出了相关探讨,其中包括性激素、信号通路、基因等。现就病毒性心肌炎所表现出的性别差异和其潜在的机制做一综述。
Abstract:
Viral myocarditis(VMC) is one of the common causes of sudden death in adolescents.The incidence and clinical manifestations of VMC have showed significant gender differences.Compared with malesthe incidence of female was lower and the disease was mild.The probability of developing dilated cardiomyopathy and even heart failure in the later stage was low,and the prognosis was good.In recent years,researchers try to explain the mechanisms underlying from various aspects including sex hormones,signaling pathways,genes and so on. This paper reviews gender bias and potential mechanisms of VMC

参考文献/References:

[1]倪荣,李丽丽病毒性心肌炎的发病机制和治疗进展[J]. 中国煤炭工业医学杂志2016,19(6):936-938.
[2]Feldman,AM,McNamara D. Myocarditis[J]. N Engl J Med,2000,343(19):1388-1398.
[3]Cocker MS,Abdel-Aty H,Strohm O,et al. Age and gender effects on the extent of myocardial involvement in acute myocarditis:a cardiovascular magnetic resonance study[J]. Heart,2009,95(23):1925-1930.
[4]Pollack A,Kontorovich AR,Fuster V,et al. Viral myocarditis—diagnosis,treatment options,and current controversies[J]. Nat Rev Cardiol,2015,12(11):670-680.
[5]Huber SA. Role of estrogen in suppressing autoimmunity in coxsackievirus B3-induced myocarditis[J]. Future Virology,2010,5(3):273-286.
[6]Woodruff JF,Woodruff JJ. Involvement of T lymphocytes in the pathogenesis of coxsackie virus B3 heart disease[J]. J Immunol,1974,113(6):1726-1734.
[7]林媛媛吴乐程,孙成勇等. 病毒性心肌炎患者外周血中Th17细胞和调节性T细胞的变化研究[J]. 中华医院感染学杂志2017,(22):98-101.
[8]Huber SA. Coxsackievirus B3-induced myocarditis:infection of females during the estrus phase of the ovarian cycle leads to activation of T regulatory cells[J]. Virology,2008,378(2):292-298.
[9]Li Z,Yue Y,Xiong S. Distinct Th17 inductions contribute to the gender bias in CVB3-induced myocarditis[J]. Cardiovascular Pathology,2013,22(5):373-382.
[10]李锋,刘利饶帮复等. γ干扰素与病毒性心肌炎[J]. 心血管病学进展2004(6):73-75.
[11]Zhou N,Yue Y,Xiong S. Sex hormone contributes to sexually dimorphic susceptibility in CVB3-induced viral myocarditis via modulating IFN-γ + NK cell production[J]. Can J Cardiol?,2018,34(4):492-501.
[12]Ivanova EA,Orekhov AN. Monocyte activation in immunopathology:cellular test for development of diagnostics and therapy[J]. J Immunol Res?,2016,2016:1-9.
[13]Li L,Jing-Ping H U,Yan Y. Estrogen promotes M2 macrophages polarization by increasing IRF4 expression[J]. Current Immunology,2013,4:23-27.
[14]Liu L,Yue Y,Xiong S. NK-derived IFN-γ/IL-4 triggers the sexually disparate polarization of macrophages in CVB3-induced myocarditis[J]. J Mol Cell Cardio,2014,76:15-25.
[15]Andreas K,Iwona B,Huber SA?. Age-associated changes in estrogen receptor ratios correlate with increased female susceptibility to coxsackievirus B3-induced myocarditis[J]. Front Immunol,2017,8:1585.
[16]Huber S. ERβ and ERα Differentially regulate NKT and Vγ4+ T-cell activation and T-regulatory cell response in coxsackievirus B3 infected mice[J]. J Clin Cell Immunol,2016,6(6):1-9.
[17]Seillet C,Laffont S,Tremollieres F,et al. The TLR-mediated response of plasmacytoid dendritic cells is positively regulated by estradiol in vivo through cell-intrinsic estrogen receptor α signaling[J]. Blood,2012,119(2):454-464.
[18]Buskiewicz IA,Koenig A,Roberts B,et al.?c-FLIP-Short reduces type I interferon production and increases viremia with coxsackievirus B3[J]. Plos One,2014,9(5):e96156.
[19]仲娇月李彩莹,梁雨亭. 病毒性心肌炎中柯萨奇B3病毒对宿主直接损伤机制的研究进展[J]. 心血管病学进展2017,38(3):355-358.
[20]Zhu X,Tang Z,Cong B,et al. Estrogens increase cystathionine-γ-lyase expression and decrease inflammation and oxidative stress in the myocardium of ovariectomized rats[J]. Menopause,2013,20(10):1084-1091.
[21]Wang F,He Q,Sun Y,et al. Female adult mouse cardiomyocytes are protected against oxidative stress[J]. Hypertension,2010,55(5):1172.
[22]Pedram A,Razandi M,Narayanan R,et al. Estrogen receptor beta signals to inhibition of cardiac fibrosis[J]. Mol Cell Endocrinol.,2016,434:57-68.
[23]Huber SA,Pfaeffle B. Differential Thl and Th2 celI responses in male and female BALB/c mice infected with Coxsackie virus group B type 3[J]. J Virol,1994,68(8):5126-5132.
[24]Wang M,Tsai BM,Kher A,et al. Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion[J]. Am J Physiol Heart Circ Physiol?,2005,288(1):H221-H226.
[25]Nikolic I,Liu D,Bell JA,et al. Treatment with an estrogen receptor-beta-selective agonist is cardioprotective[J]. J Mol Cell Cardiol?,2007,42(4):769-780.
[26]Heymans S,Schroen B,Vermeersch P,et al. Increased cardiac expression of tissue inhibitor of metalloproteinase-1 and tissue inhibitor of metalloproteinase-2 is related to cardiac fibrosis and dysfunction in the chronic pressure-overloaded human heart[J]. Circulation,2005,112(8):1136-1144.
[27]Cheung C,Marchant D,Walker KY,et al. Ablation of matrix metalloproteinase-9 increases severity of viral myocarditis in mice[J]. Circulation,2008,117(12):1574-1582.
[28]Dieplinger B,Mueller T. Soluble ST2 in heart failure[J]. Clinica Chimica Acta,2015,443:57-70.
[29]Brad G,Sophie P. The ST2/IL-33 Axis in Immune cells during inflammatory diseases[J]. Front Immunol?,2017,8:475.
[30]Coronado MJ, Bruno KA, Blauwet WA,et al. Elevated sera sST2 is associated with heart failure in men≤50?years old With Myocarditis [J]. J Am?Heart?Assoc.?,2019,8(2):e008968.
[31]Bruno KA,Mathews J,Douglass W,et al. Abstract 386:Sex differences in vitamin D alter inflammation during heart disease[J]. Circ Res,2018,123(Suppl_1):A386.
[32]Zhai X,Bai B,Yu B,et al. Coxsackievirus B3 induces autophagic response in cardiac myocytes in vivo[J]. Biochemistry(Mosc),2015,80(8):1001-1009.
[33]Zang F,Chen Y,Lin Z,et al. Autophagy is involved in regulating the immune response of dendritic cells to influenza A (H1N1) pdm09 infection[J]. Immunology,2016,148(1):56-69.
[34]Jounai N,Takeshita F,Kobiyama K,et al.?The Atg5 Atg12 conjugate associates with innate antiviral immune responses[J]. Proc Natl Acad Sci U S A,2007,104(35):14050-14055.
[35]Frisancho-Kiss S,Davis SE,Nyland JF,et al. Cutting edge:cross-regulation by TLR4 and T cell Ig mucin-3 determines sex differences in inflammatory heart disease[J]. J Immunol,2007,178(11):6710-6714.
[36]Roberts BJ,Dragon JA,Huber SA,et al. Sex-specific signaling through Toll-Like receptors 2 and 4 contributes to survival outcome of Coxsackievirus B3 infection in C57Bl/6 mice[J]. Biol Sex Differ?,2012,3(1):25.
[37]Liu G,Zhang L,Zhao Y. Modulation of immune responses through direct activation of Toll-like receptors to T cells[J]. Clin Exp Immunol.,2010,160(2):168-175.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金资助项目(81701384)
更新日期/Last Update: 2020-04-14