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糖尿病创面中的中性粒细胞胞外诱捕网和铁死亡。

Neutrophils extracellular traps and ferroptosis in diabetic wounds.

机构信息

Department of Burns and Plastic Surgery, Nanjing Drum Tower Hospital Clinical College of Jiangsu University, Nanjing, China.

Department of Emergency Surgery, The Fourth Affiliated Hospital of Jiangsu University (Zhenjiang Fourth People's Hospital), Zhenjiang, China.

出版信息

Int Wound J. 2023 Nov;20(9):3840-3854. doi: 10.1111/iwj.14231. Epub 2023 May 17.

DOI:10.1111/iwj.14231
PMID:37199077
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10588347/
Abstract

Wound healing is an extremely complex process involving multiple levels of cells and tissues. It is mainly completed through four stages: haemostasis, inflammation, proliferation, and remodelling. When any one of these stages is impaired, it may lead to delayed healing or even transformation into chronic refractory wounds. Diabetes is a kind of common metabolic disease that affects approximately 500 million people worldwide, 25% of whom develop skin ulcers that break down repeatedly and are difficult to heal, making it a growing public health problem. Neutrophils extracellular traps and ferroptosis are new types of programmed cell death identified in recent years and have been found to interact with diabetic wounds. In this paper, the normal wound healing and interfering factors of the diabetic refractory wound were outlined. The mechanism of two kinds of programmed cell death was also described, and the interaction mechanism between different types of programmed cell death and diabetic refractory wounds was discussed.

摘要

伤口愈合是一个极其复杂的过程,涉及多个层次的细胞和组织。它主要通过四个阶段完成:止血、炎症、增殖和重塑。当这些阶段中的任何一个受到损害时,可能会导致愈合延迟,甚至转化为慢性难治性伤口。糖尿病是一种常见的代谢性疾病,全球约有 5 亿人受到影响,其中 25%的人会出现皮肤溃疡,这些溃疡会反复破裂且难以愈合,成为日益严重的公共卫生问题。中性粒细胞胞外诱捕网和铁死亡是近年来发现的新型程序性细胞死亡方式,已发现它们与糖尿病性伤口相互作用。本文概述了正常伤口愈合和糖尿病难治性伤口的干扰因素。还描述了两种程序性细胞死亡的机制,并讨论了不同类型的程序性细胞死亡与糖尿病难治性伤口之间的相互作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/73ecbfe7742c/IWJ-20-3840-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/d93b2994176f/IWJ-20-3840-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/6d15d45582f5/IWJ-20-3840-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/e0e16a5d440a/IWJ-20-3840-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/73ecbfe7742c/IWJ-20-3840-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/d93b2994176f/IWJ-20-3840-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/6d15d45582f5/IWJ-20-3840-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/e0e16a5d440a/IWJ-20-3840-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/769c/10588347/73ecbfe7742c/IWJ-20-3840-g001.jpg

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本文引用的文献

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Int J Antimicrob Agents. 2023 May;61(5):106794. doi: 10.1016/j.ijantimicag.2023.106794. Epub 2023 Mar 16.
2
Platelet activation and ferroptosis mediated NETosis drives heme induced pulmonary thrombosis.血小板激活和铁死亡介导的 NETosis 驱动血红素诱导的肺血栓形成。
Biochim Biophys Acta Mol Basis Dis. 2023 Jun;1869(5):166688. doi: 10.1016/j.bbadis.2023.166688. Epub 2023 Mar 15.
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Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via the Hippo pathway.
bioRxiv. 2024 Aug 13:2024.08.12.607219. doi: 10.1101/2024.08.12.607219.
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Recent advances in molecular mechanisms of skin wound healing and its treatments.皮肤创伤愈合及其治疗的分子机制的最新进展。
Front Immunol. 2024 May 21;15:1395479. doi: 10.3389/fimmu.2024.1395479. eCollection 2024.
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Innovative Bio-based Hydrogel Microspheres Micro-Cage for Neutrophil Extracellular Traps Scavenging in Diabetic Wound Healing.用于清除糖尿病伤口愈合中中性粒细胞胞外陷阱的创新型生物基水凝胶微球微笼。
Adv Sci (Weinh). 2024 Jun;11(21):e2401195. doi: 10.1002/advs.202401195. Epub 2024 Apr 6.
6
The Role of p53 in Regulating Chronic Inflammation and PANoptosis in Diabetic Wounds.p53在调节糖尿病伤口慢性炎症和PANoptosis中的作用
Aging Dis. 2024 Feb 19;16(1):373-93. doi: 10.14336/AD.2024.0212.
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Quantitative evaluation of citrullinated fibrinogen for detection of neutrophil extracellular traps.用于检测中性粒细胞胞外陷阱的瓜氨酸化纤维蛋白原的定量评估
Immunol Res. 2024 Jun;72(3):409-417. doi: 10.1007/s12026-023-09446-5. Epub 2023 Dec 12.
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Diabet Med. 2023 Jul;40(7):e15031. doi: 10.1111/dme.15031. Epub 2023 Apr 5.
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Platelet-rich plasma promotes diabetic ulcer repair through inhibition of ferroptosis.富血小板血浆通过抑制铁死亡促进糖尿病溃疡修复。
Ann Transl Med. 2022 Oct;10(20):1121. doi: 10.21037/atm-22-4654.
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Disulfiram accelerates diabetic foot ulcer healing by blocking NET formation via suppressing the NLRP3/Caspase-1/GSDMD pathway.双硫仑通过抑制 NLRP3/Caspase-1/GSDMD 通路阻断 NET 形成加速糖尿病足溃疡愈合。
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EMBO Rep. 2022 Aug 3;23(8):e54558. doi: 10.15252/embr.202154558. Epub 2022 Jul 20.