Tumor necrosis factor-α signaling via TNFR1/p55 is deleterious whereas TNFR2/p75 signaling is protective in adult infarct myocardium.
作者信息
Kishore Raj, Tkebuchava Tengiz, Sasi Sharath P, Silver Marcy, Gilbert Hu-Ya, Yoon Young-Sup, Park Hee-Young, Thorne Tina, Losordo Douglas W, Goukassian David A
机构信息
Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL, USA.
出版信息
Adv Exp Med Biol. 2011;691:433-48. doi: 10.1007/978-1-4419-6612-4_45.
Abstract
摘要
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Tumor necrosis factor-α signaling via TNFR1/p55 is deleterious whereas TNFR2/p75 signaling is protective in adult infarct myocardium.通过肿瘤坏死因子受体1（TNFR1）/p55介导的肿瘤坏死因子-α信号传导具有有害作用，而通过肿瘤坏死因子受体2（TNFR2）/p75介导的信号传导在成年梗死心肌中具有保护作用。
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本文引用的文献
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The role of TNF-alpha receptors p55 and p75 in acute myocardial ischemia/reperfusion injury and late preconditioning.肿瘤坏死因子-α受体p55和p75在急性心肌缺血/再灌注损伤及延迟预处理中的作用
J Mol Cell Cardiol. 2008 Dec;45(6):735-41. doi: 10.1016/j.yjmcc.2008.08.014. Epub 2008 Sep 12.
2
TNFR gene-modified mesenchymal stem cells attenuate inflammation and cardiac dysfunction following MI.肿瘤坏死因子受体（TNFR）基因修饰的间充质干细胞可减轻心肌梗死后的炎症反应和心脏功能障碍。
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Tumor necrosis factor-alpha is toxic via receptor 1 and protective via receptor 2 in a murine model of myocardial infarction.在小鼠心肌梗死模型中，肿瘤坏死因子-α 通过受体 1 发挥毒性作用，通过受体 2 发挥保护作用。
Am J Physiol Heart Circ Physiol. 2007 Jul;293(1):H743-53. doi: 10.1152/ajpheart.00166.2007. Epub 2007 Apr 6.
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Tumor necrosis factor-alpha receptor p75 is required in ischemia-induced neovascularization.肿瘤坏死因子-α受体p75在缺血诱导的新生血管形成中是必需的。
Circulation. 2007 Feb 13;115(6):752-62. doi: 10.1161/CIRCULATIONAHA.106.647255. Epub 2007 Jan 29.
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Inhibition of tumor necrosis factor receptor-1-mediated pathways has beneficial effects in a murine model of postischemic remodeling.抑制肿瘤坏死因子受体-1介导的信号通路对缺血后重塑的小鼠模型具有有益作用。
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