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本文引用的文献

1
Inhibition of pro-inflammatory myeloid cell responses by short-term S100A9 blockade improves cardiac function after myocardial infarction.短期 S100A9 阻断抑制促炎髓系细胞反应可改善心肌梗死后心功能。
Eur Heart J. 2019 Aug 21;40(32):2713-2723. doi: 10.1093/eurheartj/ehz461.
2
Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges.心肌梗死的抗炎治疗：失败、希望与挑战。
Br J Pharmacol. 2018 May;175(9):1377-1400. doi: 10.1111/bph.14155. Epub 2018 Mar 4.
3
S100A8 and S100A9 Are Induced by Decreased Hydration in the Epidermis and Promote Fibroblast Activation and Fibrosis in the Dermis.S100A8 和 S100A9 由表皮水分减少诱导产生，并促进真皮成纤维细胞的激活和纤维化。
Am J Pathol. 2016 Jan;186(1):109-22. doi: 10.1016/j.ajpath.2015.09.005. Epub 2015 Nov 18.
4
Necrotic myocardial cells release damage-associated molecular patterns that provoke fibroblast activation in vitro and trigger myocardial inflammation and fibrosis in vivo.坏死的心肌细胞释放损伤相关分子模式，这些模式在体外可引发成纤维细胞活化，并在体内引发心肌炎症和纤维化。
J Am Heart Assoc. 2015 Jun 2;4(6):e001993. doi: 10.1161/JAHA.115.001993.
5
The inflammatory response in myocardial injury, repair, and remodelling.心肌损伤、修复及重塑中的炎症反应。
Nat Rev Cardiol. 2014 May;11(5):255-65. doi: 10.1038/nrcardio.2014.28. Epub 2014 Mar 25.
6
Induction of nuclear factor-κB responses by the S100A9 protein is Toll-like receptor-4-dependent.S100A9 蛋白诱导核因子-κB 反应依赖 Toll 样受体 4。
Immunology. 2012 Oct;137(2):172-82. doi: 10.1111/j.1365-2567.2012.03619.x.
7
S100A8/A9 aggravates post-ischemic heart failure through activation of RAGE-dependent NF-κB signaling.S100A8/A9 通过激活 RAGE 依赖性 NF-κB 信号加重缺血性心力衰竭。
Basic Res Cardiol. 2012 Mar;107(2):250. doi: 10.1007/s00395-012-0250-z. Epub 2012 Feb 10.
8
Enhanced expression of the S100A8/A9 complex in acute myocardial infarction patients.急性心肌梗死患者 S100A8/A9 复合物表达增强。
Circ J. 2010 Apr;74(4):741-8. doi: 10.1253/circj.cj-09-0564. Epub 2010 Feb 27.
9
The endogenous Toll-like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer.内源性Toll样受体4激动剂S100A8/S100A9（钙卫蛋白）作为感染、自身免疫和癌症的固有放大器。
J Leukoc Biol. 2009 Sep;86(3):557-66. doi: 10.1189/jlb.1008647. Epub 2009 May 18.
10
S100A8 and S100A9 mediate endotoxin-induced cardiomyocyte dysfunction via the receptor for advanced glycation end products.S100A8和S100A9通过晚期糖基化终产物受体介导内毒素诱导的心肌细胞功能障碍。
Circ Res. 2008 May 23;102(10):1239-46. doi: 10.1161/CIRCRESAHA.107.167544. Epub 2008 Apr 10.

S100A8/A9 as a therapeutic target in myocardial infarction: cellular mechanisms, molecular interactions, and translational challenges.

作者信息

Frangogiannis Nikolaos G

机构信息

The Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, USA.

出版信息

Eur Heart J. 2019 Aug 21;40(32):2724-2726. doi: 10.1093/eurheartj/ehz524.

DOI:10.1093/eurheartj/ehz524
PMID:31334753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6703152/
Abstract
摘要