Response by Nagareddy and Sreejit to Letter Regarding Article, "Retention of the NLRP3 Inflammasome-Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction-Induced Granulopoiesis".
作者信息
Nagareddy Prabhakara R, Sreejit Gopalkrishna
机构信息
Division of Cardiac Surgery, Department of Surgery, Ohio State University Wexner Medical Center, Columbus.
出版信息
Circulation. 2022 May 10;145(19):e1035-e1036. doi: 10.1161/CIRCULATIONAHA.122.059691. Epub 2022 May 9.
Abstract
摘要
相似文献
1
Response by Nagareddy and Sreejit to Letter Regarding Article, "Retention of the NLRP3 Inflammasome-Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction-Induced Granulopoiesis".纳加雷迪和斯里吉特对关于“骨髓中NLRP3炎性小体预激活的中性粒细胞的保留对心肌梗死诱导的粒细胞生成至关重要”这篇文章的信件的回应。
Circulation. 2022 May 10;145(19):e1035-e1036. doi: 10.1161/CIRCULATIONAHA.122.059691. Epub 2022 May 9.
2
Retention of the NLRP3 Inflammasome-Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction-Induced Granulopoiesis.NLRP3 炎性小体激活的中性粒细胞在骨髓中的保留对于心肌梗死诱导的粒细胞生成至关重要。
Circulation. 2022 Jan 4;145(1):31-44. doi: 10.1161/CIRCULATIONAHA.121.056019. Epub 2021 Nov 17.
3
Letter by Ren and Yang Regarding Article, "Retention of the NLRP3 Inflammasome-Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction-Induced Granulopoiesis".
Circulation. 2022 May 10;145(19):e1034. doi: 10.1161/CIRCULATIONAHA.122.059645. Epub 2022 May 9.
4
Calcium-Sensing Receptor on Neutrophil Promotes Myocardial Apoptosis and Fibrosis After Acute Myocardial Infarction via NLRP3 Inflammasome Activation.中性粒细胞钙敏感受体通过 NLRP3 炎性小体激活促进急性心肌梗死后心肌细胞凋亡和纤维化。
Can J Cardiol. 2020 Jun;36(6):893-905. doi: 10.1016/j.cjca.2019.09.026. Epub 2019 Nov 1.
5
NLRP3 Inflammasome Expression and Activation in Human Atherosclerosis.NLRP3炎症小体在人类动脉粥样硬化中的表达与激活
J Am Heart Assoc. 2016 May 20;5(5):e003031. doi: 10.1161/JAHA.115.003031.
6
Response by Sreejit and Nagareddy to Letter Regarding Article, "Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction".斯里吉特和纳加雷迪对关于文章《心肌梗死后中性粒细胞衍生的S100A8/A9增强粒细胞生成》的信件的回复
Circulation. 2020 Sep;142(9):e125-e126. doi: 10.1161/CIRCULATIONAHA.120.049408. Epub 2020 Aug 31.
7
The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury.NLRP3 炎性体在心肌成纤维细胞中上调，并介导心肌缺血再灌注损伤。
Cardiovasc Res. 2013 Jul 1;99(1):164-74. doi: 10.1093/cvr/cvt091. Epub 2013 Apr 10.
8
Chicken cathelicidin-2 promotes IL-1β secretion via the NLRP3 inflammasome pathway and serine proteases activity in LPS-primed murine neutrophils.鸡 cathelicidin-2 通过 NLRP3 炎性体途径和 LPS 预刺激的鼠中性粒细胞中的丝氨酸蛋白酶活性促进 IL-1β 的分泌。
Dev Comp Immunol. 2022 Jun;131:104377. doi: 10.1016/j.dci.2022.104377. Epub 2022 Feb 18.
9
Cholera toxin B induces interleukin-1β production from resident peritoneal macrophages through the pyrin inflammasome as well as the NLRP3 inflammasome.霍乱毒素 B 通过 pyrin 炎性小体和 NLRP3 炎性小体诱导驻留腹腔巨噬细胞产生白细胞介素-1β。
Int Immunol. 2019 Sep 18;31(10):657-668. doi: 10.1093/intimm/dxz004.
10
Tofacitinib inhibits granulocyte-macrophage colony-stimulating factor-induced NLRP3 inflammasome activation in human neutrophils.托法替布抑制粒细胞-巨噬细胞集落刺激因子诱导的人中性粒细胞中 NLRP3 炎性体的激活。
Arthritis Res Ther. 2018 Aug 29;20(1):196. doi: 10.1186/s13075-018-1685-x.
本文引用的文献
1
S100 family proteins in inflammation and beyond.S100 家族蛋白在炎症及其他方面的作用。
Adv Clin Chem. 2020;98:173-231. doi: 10.1016/bs.acc.2020.02.006. Epub 2020 Apr 17.
2
S100A9 Links Inflammation and Repair in Myocardial Infarction.S100A9 在心肌梗死中连接炎症与修复。
Circ Res. 2020 Aug 14;127(5):664-676. doi: 10.1161/CIRCRESAHA.120.315865. Epub 2020 May 21.
3
Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction.中性粒细胞衍生的 S100A8/A9 在心肌梗死后增强粒细胞生成。
Circulation. 2020 Mar 31;141(13):1080-1094. doi: 10.1161/CIRCULATIONAHA.119.043833. Epub 2020 Jan 16.
4
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.
5
Levels of S100B protein drive the reparative process in acute muscle injury and muscular dystrophy.S100B 蛋白水平驱动急性肌肉损伤和肌肉萎缩症的修复过程。
Sci Rep. 2017 Oct 2;7(1):12537. doi: 10.1038/s41598-017-12880-9.
Zotero 插件