标题:NOD2 Deficiency Protects against Cardiac Remodeling after Myocardial Infarction in Mice
作者:Li, Xiang; Li, Fengli; Chu, Yongli; Wang, Xiaojie; Zhang, Hongyu; Hu, Yanyan; Zhang, Yan; Wang, Ziying; Wei, Xinbing; Jian, Wencheng 更多
作者机构:[Li, Xiang; Li, Fengli; Wang, Xiaojie; Zhang, Yan; Wang, Ziying; Wei, Xinbing; Zhang, Xiumei; Yi, Fan] Shandong Univ, Sch Med, Dept Pharmacol, Jinan 2 更多
通讯作者:Yi, F
通讯作者地址:[Yi, F]Shandong Univ, Sch Med, Dept Pharmacol, 44 Wenhua Xi Rd, Jinan 250012, Shandong, Peoples R China.
来源:CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
出版年:2013
卷:32
期:6
页码:1857-1866
DOI:10.1159/000356618
关键词:NLR family; Matrix metalloproteinase; Cardiac dysfunction; Inflammation
摘要:Background/Aims: Although the pathogenesis of myocardial infarction (MI) is multifactorial, activation of innate immune system to induce inflammation has emerged as a key pathophysiological process in MI. NOD2, one member of the NOD-like receptor (NLR) family, plays an important role in the innate immune response. This study was to examine the role of NOD2 during MI. Methods: MI was induced by permanent ligation of the left coronary artery in wild type and NOD2(-/-) mice and cardiac fibroblasts were isolated. Results: NOD2 expression was significantly increased in myocardium in post-MI mice. NOD2 deficiency improved cardiac dysfunction and remodeling after MI as evidenced by echocardiographic analysis, reduced the levels of cytokines, inflammatory cell infiltration and matrix metalloproteinase-9 (MMP-9) activity. In vitro, we further found that NOD2 activation induced the activation of MAPK signaling pathways, production of proinflammatory mediators and MMP-9 activity in cardiac fibroblasts. Conclusions: Our studies demonstrate that NOD2 is a critical component of a signal transduction pathway that links cardiac injury by exacerbation of inflammation and MMP-9 activity. Pharmacological targeting of NOD2-mediated signaling pathways may provide a novel approach to treatment of cardiovascular diseases. Copyright (C) 2013 S. Karger AG, Basel
收录类别:SCOPUS;SCIE
WOS核心被引频次:18
Scopus被引频次:16
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84890463354&doi=10.1159%2f000356618&partnerID=40&md5=dc22c1b5fe007120d6d918c4a226fe35
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