我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

白细胞介素-33及其受体与冠心病关系的研究进展(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第2期
页码:
260-262,266
栏目:
综述
出版日期:
2012-04-25

文章信息/Info

Title:
Research advances in the relationship between IL-33 and its receptor and coronary atherosclerotic heart disease
作者:
谢 淋 综述丁世芳 审校
(广州军区武汉总医院心内科,湖北 武汉 430070)
Author(s):
XIE Lin DING Shi-fang
(Division of Cardiovascular Diseases, Wuhan General Hospital, Guangzhou Military Area Command, Wuhan 430070, Hubei, China)
关键词:
白细胞介素ST2冠状动脉粥样硬化性心脏病
Keywords:
interleukin ST2 coronary atherosclerotic heart disease
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
白细胞介素-33(IL-33)是IL-1家族的新成员,通过受体ST2介导可调节免疫炎症反应、抗心肌细胞凋亡、抑制心脏纤维化以及冠状动脉粥样硬化性心脏病的发生及发展,同时还可以减少肥胖患病风险。本文就IL-33在冠心病的形成、危险因素的控制及其预后的作用作一综述。
Abstract:
Interleukin-33 (IL-33) is a new cytokine of the IL-1 and IL-33 families. When mediated by the receptor ST2, it has the effect of regulating immune and inflammatory, decreasing myocardial apoptosis, and inhibiting myocardial fibrosis as well as the formation and development of coronary atherosclerotic heart disease. IL-33 also reduces the risk of obesity. In this paper the roles of IL-33 in the formation of coronary heart disease, control of risk factors, and prognostic evaluation of coronary heart disease were reviewed.

参考文献/References

[1]Xu D,Jiang HR,Kewin P,et al.IL-33 exacerbates antigen-induced arthritis by activating mast cells[J].Proc Natl Acad Sci USA,2008,105(31):10913-10918.

[2]Palmer G,Lipsky BP,Smithgall MD,et al.The IL-1 receptor accessory protein(AcP) is required for IL-33 signaling and soluble AcP enhances the ability of soluble ST2 to inhibit IL-33[J].Cytokine,2008,42(3):358-364.

[3] Freund C,Schmidt-Ullrich R,Baurand A,et al.Requirement of nuclear factor-kappaB in angiotensin II- and isoproterenol- induced cardiac hypertrophy in vivo[J].Circulation,2005,111(18):2319-2325.

[4]Miller AM,Xu D,Asquith DL,et al.IL-33 reduces the development of atherosclerosis[J].J Exp Med,2008,205(2):339-346.

[5]Sanasda S,Hakwno D,Higgins LJ,et al.IL-33and ST2 comprise a critical biomechanically induced and cardioprotective signaling system[J].Clin Invest,2007, 117(6):1538-1549.

[6]Martinez FO,Sica A,Mantovani A,et al.Macrophage activation and polarization[J].Front Biosci,2008,13:453-461.

[7]McLaren JE,Michael DR,Salter RC,et al.IL-33 reduces macrophage foam cell formation[J].Immunol,2010,185(2):1222-1229.

[8]Küchler AM,Pollheimer J,Balogh J,et al.Nuclear interleukin-33 is generally expressed in resting endothelium but rapidly lost upon angiogenic or proinflammatory activation[J].Am J Pathol,2008,173(4):1229- 1242.

[9]Rocha VZ,Folco EJ,Sukhova G,et al.Interferon-gamma,a Th1 cytokine,regulates fat inflammation:a role for adaptive immunity in obesity[J].J Circ Res,2008,103(5):467-476.

[10]Moro K,Yamada T,Tanabe M,et al.Innate production of T(H)2 cytokines by adipose tissue-associated c-Kit(+)Sca-1(+)lymphoid cells[J].Nature,2010,463(7280):540-544.

[11]Nishimura S,Manabe I,Nagasaki M,et al.CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity[J].Nat Med,2009,15(8):914-920.

[12]Seki K,Sanada S,Kudinova AY,et al.Interleukin-33 prevents apoptosis and improves survival after experimental myocardial infarction through ST2 signaling[J].Circ Heart Fail,2009,2(6):684-691.

[13]Dhillon OS,Narayan HK,Quinn PA,et al.Interleukin 33 and ST2 in non-ST-elevation myocardial infarction: Comparison with Global Registry of Acute Coronary Events Risk Scoring and NT-proBNP[J].Am Heart J,2011,161(6):1163-1170.

备注/Memo

备注/Memo:
收稿日期:2011-08-25.通讯作者:丁世芳,主任医师,主要从事心血管疾病的研究 Email:DSFMD yahoo.com.cn 作者简介:谢淋,硕士生 Email:2008-xielin@163.com
更新日期/Last Update: 2012-04-01