程序性细胞死亡在慢性难愈合创面炎症反应中的作用研究进展

陈雪莲; 刘琰

doi:10.3760/cma.j.cn501225-20240123-00029

程序性细胞死亡在慢性难愈合创面炎症反应中的作用研究进展

doi: 10.3760/cma.j.cn501225-20240123-00029

陈雪莲,
刘琰^,

上海交通大学医学院附属瑞金医院灼伤整形科,上海市烧伤研究所,上海　　200025

基金项目:

国家自然科学基金面上项目 82072262, 82072173

国家自然科学基金青年科学基金项目 82302796

详细信息

通讯作者:
刘琰,Email：rjliuyan@126.com

计量
- 文章访问数: 44
- HTML全文浏览量: 8
- PDF下载量: 8
- 被引次数: 0
出版历程
- 收稿日期: 2024-01-23
- 网络出版日期: 2024-10-28

Research progresses on the role of programmed cell death in the inflammatory response of chronic refractory wounds

Chen Xuelian,
Liu Yan^,

Department of Burn, Ruijin Hospital, Shanghai Burn Institute, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Funds:

General Program of National Natural Science Foundation of China 82072262, 82072173

Youth Science Fund Program of National Natural Science Foundation of China 82302796

More Information

Corresponding author: Liu Yan, Email: rjliuyan@126.com

摘要

摘要: 持续炎症反应和反复组织损伤形成慢性炎性状态,是慢性难愈合创面的重要病理特征,在慢性难愈合创面的发生发展中发挥重要致病作用。多种类型的程序性细胞死亡可释放损伤相关分子模式,触发或诱导持续炎症反应,导致组织修复失调。该综述将从产生损伤相关分子模式角度,概述程序性细胞死亡在慢性难愈合创面炎症反应中的已知作用,探讨程序性细胞死亡在慢性难愈合创面中作用及其机制的可能研究方向。
- 伤口愈合 /
- 炎症 /
- 慢性难愈合创面 /
- 程序性细胞死亡 /
- 损伤相关分子模式
Abstract: Continuous inflammatory response and repeated tissue damage lead to a chronic inflammatory state that is an important pathological feature of chronic refractory wounds, and plays an important pathogenic role in the occurrence and development of chronic refractory wounds. Multiple types of programmed cell death can release damage-associated molecular patterns, and trigger or induce sustained inflammatory responses, leading to dysregulated tissue repair. This review will outline the known role of programmed cell death in the inflammatory response of chronic refractory wounds from the perspective of generating damage-associated molecular patterns, and explore possible research directions on the role and mechanism of programmed cell death in chronic refractory wounds.
- Wound healing /
- Inflammation /
- Chronic refractory wounds /
- Programmed cell death /
- Damage-associated molecular patterns
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参考文献(46)

[1]	GongT,LiuL,JiangW,et al.DAMP-sensing receptors in sterile inflammation and inflammatory diseases[J].Nat Rev Immunol,2020,20(2):95-112.DOI: 10.1038/s41577-019-0215-7.
[2]	PeñaOA,MartinP.Cellular and molecular mechanisms of skin wound healing[J].Nat Rev Mol Cell Biol,2024,25(8):599-616.DOI: 10.1038/s41580-024-00715-1.
[3]	KlöditzK,FadeelB. Three cell deaths and a funeral: macrophage clearance of cells undergoing distinct modes of cell death[J]. Cell Death Discov,2019,5:65.DOI: 10.1038/s41420-019-0146-x.
[4]	RodriguesM,KosaricN,BonhamCA,et al.Wound healing: a cellular perspective[J].Physiol Rev,2019,99(1):665-706.DOI: 10.1152/physrev.00067.2017.
[5]	FalangaV,IsseroffRR,SoulikaAM,et al.Chronic wounds[J].Nat Rev Dis Primers,2022,8(1):50.DOI: 10.1038/s41572-022-00377-3.
[6]	RohJS,SohnDH.Damage-associated molecular patterns in inflammatory diseases[J].Immune Netw,2018,18(4):e27.DOI: 10.4110/in.2018.18.e27.
[7]	TironeM,TranNL,CeriottiC,et al.High mobility group box 1 orchestrates tissue regeneration via CXCR4[J].J Exp Med,2018,215(1):303-318.DOI: 10.1084/jem.20160217.
[8]	TangD,KangR,ZehHJ,et al.The multifunctional protein HMGB1: 50 years of discovery[J].Nat Rev Immunol,2023,23(12):824-841.DOI: 10.1038/s41577-023-00894-6.
[9]	VorobjevaNV,ChernyakBV.NETosis: molecular mechanisms, role in physiology and pathology[J].Biochemistry (Mosc),2020,85(10):1178-1190.DOI: 10.1134/S0006297920100065.
[10]	LiuD,YangP,GaoM,et al.NLRP3 activation induced by neutrophil extracellular traps sustains inflammatory response in the diabetic wound[J].Clin Sci (Lond),2019,133(4):565-582.DOI: 10.1042/CS20180600.
[11]	AndertonH,WicksIP,SilkeJ.Cell death in chronic inflammation: breaking the cycle to treat rheumatic disease[J].Nat Rev Rheumatol,2020,16(9):496-513.DOI: 10.1038/s41584-020-0455-8.
[12]	GreenDR,FergusonT,ZitvogelL,et al.Immunogenic and tolerogenic cell death[J].Nat Rev Immunol,2009,9(5):353-363.DOI: 10.1038/nri2545.
[13]	ChenX,KangR,KroemerG,et al.Ferroptosis in infection, inflammation, and immunity[J]. J Exp Med,2021,218(6):e20210518.DOI: 10.1084/jem.20210518.
[14]	LiS,LiY,WuZ,et al.Diabetic ferroptosis plays an important role in triggering on inflammation in diabetic wound[J].Am J Physiol Endocrinol Metab,2021,321(4):E509-E520.DOI: 10.1152/ajpendo.00042.2021.
[15]	WuX,HeW,MuX,et al.Macrophage polarization in diabetic wound healing[J/OL].Burns Trauma,2022,10:tkac051[2024-01-23].https://pubmed.ncbi.nlm.nih.gov/36601058/.DOI: 10.1093/burnst/tkac051.
[16]	JustynskiO,BridgesK,KrauseW,et al.Apoptosis recognition receptors regulate skin tissue repair in mice[J].Elife,2023,12:e86269.DOI: 10.7554/eLife.86269.
[17]	MartinSJ,HenryCM,CullenSP.A perspective on mammalian caspases as positive and negative regulators of inflammation[J].Mol Cell,2012,46(4):387-397.DOI: 10.1016/j.molcel.2012.04.026.
[18]	孙炳伟,黄佳敏.中性粒细胞生理与病理生理作用再认识[J].中华烧伤与创面修复杂志,2022,38(2):109-113.DOI: 10.3760/cma.j.cn501120-20211122-00391.
[19]	UderhardtS,MartinsAJ,TsangJS,et al.Resident macrophages cloak tissue microlesions to prevent neutrophil-driven inflammatory damage[J].Cell,2019,177(3):541-555.e17.DOI: 10.1016/j.cell.2019.02.028.
[20]	MoriokaS,MaueröderC,RavichandranKS.Living on the edge: efferocytosis at the interface of homeostasis and pathology[J].Immunity,2019,50(5):1149-1162.DOI: 10.1016/j.immuni.2019.04.018.
[21]	Boada-RomeroE,MartinezJ,HeckmannBL,et al.The clearance of dead cells by efferocytosis[J].Nat Rev Mol Cell Biol,2020,21(7):398-414.DOI: 10.1038/s41580-020-0232-1.
[22]	MaschalidiS,MehrotraP,KeçeliBN,et al.Targeting SLC7A11 improves efferocytosis by dendritic cells and wound healing in diabetes[J].Nature,2022,606(7915):776-784.DOI: 10.1038/s41586-022-04754-6.
[23]	AryaAK,TripathiR,KumarS,et al.Recent advances on the association of apoptosis in chronic non healing diabetic wound[J].World J Diabetes,2014,5(6):756-762.DOI: 10.4239/wjd.v5.i6.756.
[24]	TingAT,BertrandMJM.More to life than NF-κB in TNFR1 signaling[J].Trends Immunol,2016,37(8):535-545.DOI: 10.1016/j.it.2016.06.002.
[25]	van LooG,BertrandMJM.Death by TNF: a road to inflammation[J].Nat Rev Immunol,2023,23(5):289-303.DOI: 10.1038/s41577-022-00792-3.
[26]	ZhangX,FanC,ZhangH,et al.MLKL and FADD are critical for suppressing progressive lymphoproliferative disease and activating the NLRP3 inflammasome[J].Cell Rep,2016,16(12):3247-3259.DOI: 10.1016/j.celrep.2016.06.103.
[27]	KiturK,WachtelS,BrownA,et al.Necroptosis promotes Staphylococcus aureus clearance by inhibiting excessive inflammatory signaling[J].Cell Rep,2016,16(8):2219-2230.DOI: 10.1016/j.celrep.2016.07.039.
[28]	CaoY,HarveyBP,JinL,et al.Therapeutic TNF inhibitors exhibit differential levels of efficacy in accelerating cutaneous wound healing[J].JID Innov,2024,4(1):100250.DOI: 10.1016/j.xjidi.2023.100250.
[29]	InjarabianL,WillenborgS,WelckerD,et al.FADD- and RIPK3-mediated cell death ensures clearance of Ly6C^high wound macrophages from damaged tissue[J].J Invest Dermatol,2024,144(1):152-164.e7.DOI: 10.1016/j.jid.2023.06.203.
[30]	何家乐,董鸿斐,黄茜,等.细胞焦亡在糖尿病创面愈合中的作用研究进展[J].中华烧伤与创面修复杂志,2024,40(8):785-791.DOI: 10.3760/cma.j.cn501225-20230829-00068.
[31]	FeniniG,GrossiS,ContassotE,et al.Genome editing of human primary keratinocytes by CRISPR/Cas9 reveals an essential role of the NLRP1 inflammasome in UVB sensing[J].J Invest Dermatol,2018,138(12):2644-2652.DOI: 10.1016/j.jid.2018.07.016.
[32]	FeniniG,KarakayaT,HennigP,et al.The NLRP1 inflammasome in human skin and beyond[J].Int J Mol Sci,2020,21(13):4788.DOI: 10.3390/ijms21134788.
[33]	MutuaV,GershwinLJ.A review of neutrophil extracellular traps (NETs) in disease: potential anti-NETs therapeutics[J].Clin Rev Allergy Immunol,2021,61(2):194-211.DOI: 10.1007/s12016-020-08804-7.
[34]	SabbatiniM,MagnelliV,RenòF.NETosis in wound healing: when enough is enough[J].Cells,2021,10(3):494.DOI: 10.3390/cells10030494.
[35]	LeeYS,KangSU,LeeMH,et al.GnRH impairs diabetic wound healing through enhanced NETosis[J].Cell Mol Immunol,2020,17(8):856-864.DOI: 10.1038/s41423-019-0252-y.
[36]	ZhuY,XiaX,HeQ,et al.Diabetes-associated neutrophil NETosis: pathogenesis and interventional target of diabetic complications[J].Front Endocrinol (Lausanne),2023,14:1202463.DOI: 10.3389/fendo.2023.1202463.
[37]	TangD,ChenX,KangR,et al.Ferroptosis: molecular mechanisms and health implications[J].Cell Res,2021,31(2):107-125.DOI: 10.1038/s41422-020-00441-1.
[38]	ZhengJ,ConradM.The metabolic underpinnings of ferroptosis[J].Cell Metab,2020,32(6):920-937.DOI: 10.1016/j.cmet.2020.10.011.
[39]	杨岚婷,徐涛,杨福情,等.转铁蛋白受体对铁过载所致大鼠心肌细胞铁死亡的作用及其机制[J].解放军医学杂志,2022,47(8):781-788.DOI: 10.11855/j.issn.0577-7402.2022.08.0781.
[40]	WangF,HeJ,XingR,et al.Molecular mechanisms of ferroptosis and their role in inflammation[J].Int Rev Immunol,2023,42(1):71-81.DOI: 10.1080/08830185.2021.2016739.
[41]	KapralovAA,YangQ,DarHH,et al.Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death[J].Nat Chem Biol,2020,16(3):278-290.DOI: 10.1038/s41589-019-0462-8.
[42]	MatsushitaM,FreigangS,SchneiderC,et al.T cell lipid peroxidation induces ferroptosis and prevents immunity to infection[J].J Exp Med,2015,212(4):555-568.DOI: 10.1084/jem.20140857.
[43]	YangW,WangX,XuL,et al.LOX inhibitor HOEC interfered arachidonic acid metabolic flux in collagen-induced arthritis rats[J].Am J Transl Res,2018,10(8):2542-2554.
[44]	ChhabraR,SahaA,ChamaniA,et al.Iron pathways and iron chelation approaches in viral, microbial, and fungal infections[J].Pharmaceuticals (Basel),2020,13(10):275.DOI: 10.3390/ph13100275.
[45]	WlaschekM,SinghK,SindrilaruA,et al.Iron and iron-dependent reactive oxygen species in the regulation of macrophages and fibroblasts in non-healing chronic wounds[J].Free Radic Biol Med,2019,133:262-275.DOI: 10.1016/j.freeradbiomed.2018.09.036.
[46]	GaoSQ,ChangC,LiJJ,et al.Co-delivery of deferoxamine and hydroxysafflor yellow A to accelerate diabetic wound healing via enhanced angiogenesis[J].Drug Deliv,2018,25(1):1779-1789.DOI: 10.1080/10717544.2018.1513608.