炎症反应在心梗后心衰发病过程中的作用研究进展

刘雪岩; 李成花; 杨萍

doi:10.3969/j.issn.1674-4500.2017.01.24

炎症反应在心梗后心衰发病过程中的作用研究进展

doi: 10.3969/j.issn.1674-4500.2017.01.24

吉林大学中日联谊医院心血管内科，长春吉林 130033

基金项目:

国家自然科学基金 81570360

详细信息

作者简介:
刘雪岩，E-mail: 349964145@qq.com

通讯作者:
杨萍，E-mail: pyang@jlu.edu.cn

计量
- 文章访问数: 611
- HTML全文浏览量: 649
- PDF下载量: 26
- 被引次数: 0
出版历程
- 收稿日期: 2016-07-15
- 刊出日期: 2017-01-01

Progress in effects and regulation of inflammatory response in post-infarction heart failure

Department of Internal Medicine Cardiovascular, Union Hospital of China and Japan affiliated to Jilin University,Changchun 130033, China

摘要

摘要: 心梗后心衰是慢性心力衰竭中最常见的类型，近年研究发现炎症反应迅速、持续的激活是心梗后心衰的重要特征。适当的炎症反应可以减少心肌梗死范围，促进瘢痕形成及缺血心肌的恢复，而炎症反应过度、持久激活可促进心脏扩大、心功能不全及心力衰竭。心肌梗死后心肌细胞释放坏死物质，通过激活 TLR 介导的通路、补体系统以及 ROS 诱导的通路调控 NF-κB 相关通路，激活体内固有免疫。同时中性粒细胞、单核细胞、巨噬细胞等多种细胞参与了炎症过程。如何通过调控心梗后心衰过程中的炎症反应从而抑制病理性重构为心衰的治疗提供了新的方向。本文从炎症反应激活过程中的细胞基础及相关通路两方面，对炎症反应在心梗后心衰过程中的作用及机制做一系统综述，为进一步研究心衰过程中炎症反应的作用及抗炎治疗提供参考。
- 心力衰竭 /
- 炎症反应 /
- 心肌梗死 /
- 免疫
Abstract: Myocardial infarction is the most common cause that induces heart failure. Recent studies have identified that instant and prolonged activation of inflammatory response is a key character of post-infarction heart failure. Inflammatory response to some degree can promote wound healing, scar formation and recovery of ischemic myocardium, but excessive inflammation could play an important role in the development of chamber dilation, systolic dysfunction and heart failure. Extensive necrosis in the infarcted myocardium triggers the innate immune response through stimulating Toll-Like Receptor (TLR) mediated signaling, activating the complement cascade and reactive oxygen species (ROS) pathway, and regulating the Nuclear Factor (NF)- κB system. Neutrophils, mononuclear cells, macrophages and other kinds of cells play essential roles in inf lammation. How to control inflammation to suppress pathological remodeling is an important issue to be considered in developing new treatment for heart failure. This review summarizes the roles of related cells and signal pathways in the pathophysiological mechanisms of inflammation in myocardial induced heart failure in order to provide references for further study in the effects of inflammation and anti-inflammatory therapies in heart failure.
- heart failure /
- inflammatory response /
- myocardial infarction /
- immunity

HTML全文

参考文献(20)

[1]	Christia P, Frangogiannis NG. Targeting inflammatory pathways in myocardial infarction[J]. Eur J Clin Invest, 2013, 43(9): 986-95. doi: 10.1111/eci.2013.43.issue-9
[2]	Frangogiannis NG. The inflammatory response in myocardial injury, repair, and remodelling[J]. Nat Rev Cardiol, 2014, 11(5):255-65. doi: 10.1038/nrcardio.2014.28
[3]	Ding HS, Yang J, Chen P, et al. The HMGB1-TLR4 axis contributes to myocardial ischemia/reperfusion injury via regulation of cardiomyocyte apoptosis[J]. Gene, 2013, 527(1): 389-93. doi: 10.1016/j.gene.2013.05.041
[4]	Timmers L, Pasterkamp G, de Hoog VC, et al. The innate immune response in reperfused myocardium[J]. Cardiovasc Res, 2012, 94(2): 276-83. doi: 10.1093/cvr/cvs018
[5]	Souders CA, Bowers SL, Baudino TA. Cardiac fibroblast: the Renaissance cell [J]. Circ Res, 2009, 105(12): 1164-76. doi: 10.1161/CIRCRESAHA.109.209809
[6]	Kawaguchi M, Takahashi M, Hata TA, et al. Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury[J]. Circulation, 2011, 123(6): 594-9. doi: 10.1161/CIRCULATIONAHA.110.982777
[7]	Bujak M, Dobaczewski M, Gonzalez QC, et al. Induction of the CXC chemokine Interferon-gamma-Inducible protein 10 regulates the reparative response following myocardial infarction[J]. Circ Res, 2009, 105(10): 973-83. doi: 10.1161/CIRCRESAHA.109.199471
[8]	Bournazou I, Pound JD, Duffin R, et al. Apoptotic human cells inhibit migration of granulocytes via release of lactoferrin[J]. J Clin Invest, 2009, 119(1): 20-32. http://cn.bing.com/academic/profile?id=e633ad94cd1d7bf6889dbca6a16daeaf&encoded=0&v=paper_preview&mkt=zh-cn
[9]	Williams MR, Azcutia V, Newton G, et al. Emerging mechanisms of neutrophil recruitment across endothelium[J]. Trends Immunol,2011, 32(10): 461-9. doi: 10.1016/j.it.2011.06.009
[10]	Nording HM, Seizer P, Langer HF. Platelets in inflammation and atherogenesis[J]. Front Immunol, 2015, 6(11): 98-103. http://cn.bing.com/academic/profile?id=de6a1e362b314234ad4f0f1f28c68589&encoded=0&v=paper_preview&mkt=zh-cn
[11]	Del CI, Cruz M, Zhang H, et al. Platelet activation leads to activation and propagation of the complement system[J]. J Exp Med, 2005, 201(6): 871-9. doi: 10.1084/jem.20041497
[12]	Riad A, Jäger S, Sobirey M, et al. Toll-like receptor-4 modulates survival by induction of left ventricular remodeling after myocardial infarction in mice[J]. J Immunol, 2008, 180(10):6954-61. doi: 10.4049/jimmunol.180.10.6954
[13]	Pepys MB, Hirschfield GM, Tennent GA, et al. Targeting C-reactive protein for the treatment of cardiovascular disease[J]. Nature, 2006,440(8): 1217-21. http://cn.bing.com/academic/profile?id=57c6b54714e9b6567dfae1c4b56ae5b2&encoded=0&v=paper_preview&mkt=zh-cn
[14]	Salio M, Chimenti S, de Angelis N, et al. Cardioprotective function of the long pentraxin PTX3 in acute myocardial infarction[J]. Circulation, 2008, 117(8): 1055-64. doi: 10.1161/CIRCULATIONAHA.107.749234
[15]	Granger CB, Mahaffey KW, Weaver WD, et al. Pexelizumab,an anti-C5 complement antibody,as adjunctive therapy to primary percutaneous coronary intervention in acute myocardial infarction: the complement inhibition in Myocardial infarction treated with Angioplasty trial [J]. Circulation, 2003, 108(10): 1184-90. doi: 10.1161/01.CIR.0000087447.12918.85
[16]	Mahaffey KW, Granger CB, Nicolau JC, et al. Effect of pexelizumab,an anti-C5 complement antibody,as adjunctive therapy to fibrinolysis in acute myocardial infarction:the complement inhibition in myocardial infarction treated with thrombolytics trial[J]. Circulation, 2003, 108(10): 1176-83. doi: 10.1161/01.CIR.0000087404.53661.F8
[17]	Nian M, Lee P, Khaper N, et al. Inflammatory cytokines and postmyocardial infarction remodeling[J]. Circ Res, 2004, 94(12):1543-53. doi: 10.1161/01.RES.0000130526.20854.fa
[18]	Gordon JW, Shaw JA, Kirshenbaum LA. Multiple facets of NF-kappaB in the heart:to be or not to NF-kappaB[J]. Circ Res,2011, 108(9): 1122-32. doi: 10.1161/CIRCRESAHA.110.226928
[19]	Moss NC, Stansfield WE, Willis MS, et al. IKK beta inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury[J]. Am J Physiol Heart Circ Physiol,2007, 293(4): H2248-53. doi: 10.1152/ajpheart.00776.2007
[20]	Misra A, Haudek SB, Knuefermann P, et al. Nuclear factor-kappa B protects the adult cardiac myocyte against ischemia-induced apoptosis in a murine model of acute myocardial infarction[J]. Circulation, 2003, 108(25): 3075-8. doi: 10.1161/01.CIR.0000108929.93074.0B

施引文献

资源附件(0)

访问统计

点击查看大图

计量

文章访问数: 611
HTML全文浏览量: 649
PDF下载量: 26
被引次数: 0

姓名
邮箱
手机号码
标题
留言内容
验证码

留言板

炎症反应在心梗后心衰发病过程中的作用研究进展

doi: 10.3969/j.issn.1674-4500.2017.01.24

作者简介:
刘雪岩，E-mail: 349964145@qq.com

通讯作者:
杨萍，E-mail: pyang@jlu.edu.cn

计量

Progress in effects and regulation of inflammatory response in post-infarction heart failure

计量

目录

留言板

炎症反应在心梗后心衰发病过程中的作用研究进展

doi: 10.3969/j.issn.1674-4500.2017.01.24

作者简介: 刘雪岩，E-mail: 349964145@qq.com

通讯作者: 杨 萍，E-mail: pyang@jlu.edu.cn

计量

出版历程

Progress in effects and regulation of inflammatory response in post-infarction heart failure

计量

出版历程

目录

作者简介:
刘雪岩，E-mail: 349964145@qq.com

通讯作者:
杨萍，E-mail: pyang@jlu.edu.cn