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1
NETs and traps delay wound healing in diabetes.中性粒细胞胞外诱捕网(NETs)和陷阱会延迟糖尿病患者的伤口愈合。
Trends Endocrinol Metab. 2015 Sep;26(9):451-2. doi: 10.1016/j.tem.2015.07.004. Epub 2015 Jul 31.
2
Diabetes primes neutrophils to undergo NETosis, which impairs wound healing.糖尿病使中性粒细胞易于发生中性粒细胞胞外陷阱形成,从而损害伤口愈合。
Nat Med. 2015 Jul;21(7):815-9. doi: 10.1038/nm.3887. Epub 2015 Jun 15.
3
GnRH impairs diabetic wound healing through enhanced NETosis.促性腺激素释放激素通过增强中性粒细胞胞外陷阱形成损害糖尿病伤口愈合。
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NETosis Delays Diabetic Wound Healing in Mice and Humans.中性粒细胞胞外诱捕网形成延迟糖尿病小鼠和人类伤口愈合。
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Sweet NETs, Bitter Wounds.甜蜜的 NETs,痛苦的伤口。
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The W620 Polymorphism in PTPN22 Disrupts Its Interaction With Peptidylarginine Deiminase Type 4 and Enhances Citrullination and NETosis.W620 多态性破坏了 PTPN22 与肽基精氨酸脱亚氨酶 4 的相互作用,增强了瓜氨酸化和 NETosis。
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Improving the Wound Healing Process: Pivotal role of Mesenchymal stromal/stem Cells and Immune Cells.改善伤口愈合过程:间充质基质/干细胞和免疫细胞的关键作用。
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TGF-β-driven LIF expression influences neutrophil extracellular traps (NETs) and contributes to peritoneal metastasis in gastric cancer.TGF-β 驱动的 LIF 表达影响中性粒细胞胞外陷阱(NETs),并有助于胃癌的腹膜转移。
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Bioinformatics analysis identifies TGF-β signaling pathway-associated molecular subtypes and gene signature in diabetic foot.生物信息学分析确定糖尿病足中与转化生长因子-β信号通路相关的分子亚型和基因特征。
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Inhibition of neutrophil extracellular trap formation alleviates vascular dysfunction in type 1 diabetic mice.抑制中性粒细胞胞外诱捕网形成可减轻 1 型糖尿病小鼠的血管功能障碍。
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Reduction of neutrophil extracellular traps accelerates inflammatory resolution and increases bone formation on titanium implants.减少中性粒细胞胞外陷阱可加速炎症消退并增加钛植入物上的骨形成。
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Novel neutrophil extracellular trap-related mechanisms in diabetic wounds inspire a promising treatment strategy with hypoxia-challenged small extracellular vesicles.糖尿病伤口中与中性粒细胞胞外诱捕网相关的新机制激发了一种利用低氧刺激的小细胞外囊泡的前景广阔的治疗策略。
Bioact Mater. 2023 Apr 14;27:257-270. doi: 10.1016/j.bioactmat.2023.04.007. eCollection 2023 Sep.
9
Colonizing microbiota is associated with clinical outcomes in diabetic wound healing.定植菌群与糖尿病创面愈合的临床结局相关。
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10
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本文引用的文献

1
Diabetes primes neutrophils to undergo NETosis, which impairs wound healing.糖尿病使中性粒细胞易于发生中性粒细胞胞外陷阱形成,从而损害伤口愈合。
Nat Med. 2015 Jul;21(7):815-9. doi: 10.1038/nm.3887. Epub 2015 Jun 15.
2
PAD4-deficiency does not affect bacteremia in polymicrobial sepsis and ameliorates endotoxemic shock.肽基精氨酸脱亚氨酶4(PAD4)缺陷不影响多重微生物败血症中的菌血症,并可改善内毒素血症性休克。
Blood. 2015 Mar 19;125(12):1948-56. doi: 10.1182/blood-2014-07-587709. Epub 2015 Jan 26.
3
NETosis is induced by high glucose and associated with type 2 diabetes.中性粒细胞胞外陷阱形成由高血糖诱导,并与2型糖尿病相关。
Acta Diabetol. 2015 Jun;52(3):497-503. doi: 10.1007/s00592-014-0676-x. Epub 2014 Nov 12.
4
Increased neutrophil elastase and proteinase 3 and augmented NETosis are closely associated with β-cell autoimmunity in patients with type 1 diabetes.中性粒细胞弹性蛋白酶和蛋白酶 3 增加以及 NETosis 增强与 1 型糖尿病患者的 β 细胞自身免疫密切相关。
Diabetes. 2014 Dec;63(12):4239-48. doi: 10.2337/db14-0480. Epub 2014 Aug 4.
5
Increased DNase I activity in diabetes might be associated with injury of pancreas.糖尿病中脱氧核糖核酸酶I活性增加可能与胰腺损伤有关。
Mol Cell Biochem. 2014 Aug;393(1-2):23-32. doi: 10.1007/s11010-014-2043-1. Epub 2014 Mar 28.
6
Citrullination regulates pluripotency and histone H1 binding to chromatin.瓜氨酸化调控多能性和组蛋白 H1 与染色质的结合。
Nature. 2014 Mar 6;507(7490):104-8. doi: 10.1038/nature12942. Epub 2014 Jan 26.
7
Negative regulation of the peptidylarginine deiminase type IV promoter by NF-κB in human myeloid cells.人髓样细胞中 NF-κB 对肽基精氨酸脱亚氨酶 IV 启动子的负调控。
Gene. 2014 Jan 1;533(1):123-31. doi: 10.1016/j.gene.2013.09.108. Epub 2013 Oct 16.
8
Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase.中性粒细胞通过分泌弹性蛋白酶介导高脂饮食喂养的小鼠胰岛素抵抗。
Nat Med. 2012 Sep;18(9):1407-12. doi: 10.1038/nm.2885.
9
P-selectin glycoprotein ligand-1 regulates adhesive properties of the endothelium and leukocyte trafficking into adipose tissue.P-选择素糖蛋白配体-1 调节内皮细胞的黏附特性和白细胞向脂肪组织的迁移。
Circ Res. 2010 Aug 6;107(3):388-97. doi: 10.1161/CIRCRESAHA.110.218651. Epub 2010 Jun 17.
10
Cellular and molecular basis of wound healing in diabetes.糖尿病伤口愈合的细胞和分子基础
J Clin Invest. 2007 May;117(5):1219-22. doi: 10.1172/JCI32169.

中性粒细胞胞外诱捕网(NETs)和陷阱会延迟糖尿病患者的伤口愈合。

NETs and traps delay wound healing in diabetes.

作者信息

Roth Flach Rachel J, Czech Michael P

机构信息

Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

出版信息

Trends Endocrinol Metab. 2015 Sep;26(9):451-2. doi: 10.1016/j.tem.2015.07.004. Epub 2015 Jul 31.

DOI:10.1016/j.tem.2015.07.004
PMID:26239304
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4558202/
Abstract

Diabetes is associated with dire peripheral sequelae including foot ulcers and amputations. A recent article by Wong et al. demystifies this connection by demonstrating that the neutrophil defense mechanism of extruding decondensed chromatin, termed NETosis, mediates delayed wound healing in diabetes and provides a therapeutic strategy for this indication.

摘要

糖尿病与包括足部溃疡和截肢在内的严重外周后遗症相关。Wong等人最近发表的一篇文章揭示了这种关联,他们证明了中性粒细胞挤出解聚染色质的防御机制(称为中性粒细胞胞外陷阱形成)介导了糖尿病患者伤口愈合延迟,并为该适应症提供了一种治疗策略。