Myocardial pressure overload induces systemic inflammation through endothelial cell IL-33
出版年份 2015 全文链接
标题
Myocardial pressure overload induces systemic inflammation through endothelial cell IL-33
作者
关键词
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出版物
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 112, Issue 23, Pages 7249-7254
出版商
Proceedings of the National Academy of Sciences
发表日期
2015-05-05
DOI
10.1073/pnas.1424236112
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy
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- Interleukin-33 Prevents Apoptosis and Improves Survival After Experimental Myocardial Infarction Through ST2 Signaling
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- Nuclear Interleukin-33 Is Generally Expressed in Resting Endothelium but Rapidly Lost upon Angiogenic or Proinflammatory Activation
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- IL-33 reduces the development of atherosclerosis
- (2008) Ashley M. Miller et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Nonmyocardial Production of ST2 Protein in Human Hypertrophy and Failure Is Related to Diastolic Load
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- The IL-1-Like Cytokine IL-33 Is Constitutively Expressed in the Nucleus of Endothelial Cells and Epithelial Cells In Vivo: A Novel ‘Alarmin’?
- (2008) Christine Moussion et al. PLoS One
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