留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

代谢重塑及蛋白酰化修饰在瘢痕疙瘩中的作用研究进展

穆泽兰 滕泳翔 张键 白南 付妍婕

穆泽兰, 滕泳翔, 张键, 等. 代谢重塑及蛋白酰化修饰在瘢痕疙瘩中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2024, 40(6): 589-593. DOI: 10.3760/cma.j.cn501225-20231207-00229.
引用本文: 穆泽兰, 滕泳翔, 张键, 等. 代谢重塑及蛋白酰化修饰在瘢痕疙瘩中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2024, 40(6): 589-593. DOI: 10.3760/cma.j.cn501225-20231207-00229.
Mu ZL,Teng YX,Zhang J,et al.Research advances on the roles of metabolic remodeling and protein acylation modification in keloids[J].Chin J Burns Wounds,2024,40(6):589-593.DOI: 10.3760/cma.j.cn501225-20231207-00229.
Citation: Mu ZL,Teng YX,Zhang J,et al.Research advances on the roles of metabolic remodeling and protein acylation modification in keloids[J].Chin J Burns Wounds,2024,40(6):589-593.DOI: 10.3760/cma.j.cn501225-20231207-00229.

代谢重塑及蛋白酰化修饰在瘢痕疙瘩中的作用研究进展

doi: 10.3760/cma.j.cn501225-20231207-00229
基金项目: 

山东省自然科学基金面上项目 ZR2021MH338

详细信息
    通讯作者:

    付妍婕,Email:zcfyjzzy@163.com

Research advances on the roles of metabolic remodeling and protein acylation modification in keloids

Funds: 

General Program of Natural Science Foundation of Shandong Province of China ZR2021MH338

More Information
  • 摘要: 瘢痕疙瘩是一种常见的皮肤疾病,其发生机制尚不完全清楚,但已有证据表明,多种因素如遗传、种族、年龄、性别、激素、感染、免疫、氧化应激等都可能与瘢痕疙瘩的发生相关。代谢重塑及蛋白酰化修饰作为2种重要的生物学过程,在多种皮肤相关疾病中发挥着重要作用。基于此,该文综述代谢重塑及蛋白酰化修饰在瘢痕疙瘩中的作用及这2种生物学过程的相互关系,并探讨靶向这2种生物学过程在预防和治疗瘢痕疙瘩中的应用前景。

     

  • 参考文献(48)

    [1] 王文波.瘢痕疙瘩最新研究进展[J].组织工程与重建外科杂志,2018,14(6):357-360.DOI: 10.3969/j.issn.1673-0364.2018.06.016.
    [2] 杨丽Twist促进乳腺癌细胞能量代谢重塑的作用及相关机制研究重庆重庆医科大学2015DOI:10.7666/d.D791520

    杨丽.Twist促进乳腺癌细胞能量代谢重塑的作用及相关机制研究[D].重庆:重庆医科大学,2015.DOI:10.7666/d.D791520.

    [3] SunL,ZhangH,GaoP.Metabolic reprogramming and epigenetic modifications on the path to cancer[J].Protein Cell,2022,13(12):877-919.DOI: 10.1007/s13238-021-00846-7.
    [4] MentchSJ,MehrmohamadiM,HuangL,et al.Histone methylation dynamics and gene regulation occur through the sensing of one-carbon metabolism[J].Cell Metab,2015,22(5):861-873.DOI: 10.1016/j.cmet.2015.08.024.
    [5] KaelinWGJr,McKnightSL.Influence of metabolism on epigenetics and disease[J].Cell,2013,153(1):56-69.DOI: 10.1016/j.cell.2013.03.004.
    [6] 李泽炎,于颖,沈嘉伦,等.HIF-1α参与瘢痕疙瘩生成机制的研究现状[J].中国美容整形外科杂志,2021,32(11):673-677.DOI: 10.3969/j.issn.1673-7040.2021.11.010.
    [7] 王其飞瘢痕疙瘩成纤维细胞在低氧下的糖代谢特点及作用机制北京北京大学医学部2021DOI:10.44277/d.cnki.gbdyx.2021.000068

    王其飞.瘢痕疙瘩成纤维细胞在低氧下的糖代谢特点及作用机制[D].北京:北京大学医学部,2021.DOI:10.44277/d.cnki.gbdyx.2021.000068.

    [8] VaupelP,MulthoffG.Fatal alliance of hypoxia-/HIF-1α-driven microenvironmental traits promoting cancer progression[J].Adv Exp Med Biol,2020,1232:169-176.DOI: 10.1007/978-3-030-34461-0_21.
    [9] LiQ,QinZ,NieF,et al.Metabolic reprogramming in keloid fibroblasts: aerobic glycolysis and a novel therapeutic strategy[J].Biochem Biophys Res Commun,2018,496(2):641-647.DOI: 10.1016/j.bbrc.2018.01.068.
    [10] 雷睿缺氧诱导因子-1α及其相关信号通路促进瘢痕疙瘩形成的作用机制研究杭州浙江大学2017

    雷睿.缺氧诱导因子-1α及其相关信号通路促进瘢痕疙瘩形成的作用机制研究[D].杭州:浙江大学,2017.

    [11] HuangC,OgawaR.Roles of lipid metabolism in keloid development[J].Lipids Health Dis,2013,12:60.DOI: 10.1186/1476-511X-12-60.
    [12] 张慧君.脂类代谢对瘢痕疙瘩作用的研究进展[J]. 医药前沿,2016,6(7):5-6.
    [13] AndrewsD,GodsonC.Lipoxins and synthetic lipoxin mimetics: therapeutic potential in renal diseases[J].Biochim Biophys Acta Mol Cell Biol Lipids,2021,1866(8):158940.DOI: 10.1016/j.bbalip.2021.158940.
    [14] OwenB,GuiryPJ.A general synthesis of aromatic and heteroaromatic lipoxin B4 analogues[J].Org Biomol Chem,2023,21(41):8294-8300.DOI: 10.1039/d3ob01076g.
    [15] MilesEA,AllenE,CalderPC.In vitro effects of eicosanoids derived from different 20-carbon fatty acids on production of monocyte-derived cytokines in human whole blood cultures[J].Cytokine,2002,20(5):215-223.DOI: 10.1006/cyto.2002.2007.
    [16] ShanM,LiuH,HaoY,et al.Metabolomic profiling reveals that 5-hydroxylysine and 1-methylnicotinamide are metabolic indicators of keloid severity[J].Front Genet,2022,12:804248.DOI: 10.3389/fgene.2021.804248.
    [17] SakakiH,MatsumiyaT,KusumiA,et al.Interleukin-1β induces matrix metalloproteinase-1 expression in cultured human gingival fibroblasts: role of cyclooxygenase-2 and prostaglandin E2[J].Oral Dis,2004,10(2):87-93.DOI: 10.1046/j.1354-523x.2003.00982.x.
    [18] LouwL.Keloids in rural black South Africans. Part 3: a lipid model for the prevention and treatment of keloid formations[J].Prostaglandins Leukot Essent Fatty Acids,2000,63(5):255-262.DOI: 10.1054/plef.2000.0209.
    [19] HendersonJ,DuffyL,StrattonR,et al.Metabolic reprogramming of glycolysis and glutamine metabolism are key events in myofibroblast transition in systemic sclerosis pathogenesis[J].J Cell Mol Med,2020,24(23):14026-14038.DOI: 10.1111/jcmm.16013.
    [20] HuY,ZhouX,ChenL,et al.Landscape of circulating metabolic fingerprinting for keloid[J].Front Immunol,2022,13:1005366.DOI: 10.3389/fimmu.2022.1005366.
    [21] StevensonAW,DengZ,AllahhamA,et al.The epigenetics of keloids[J].Exp Dermatol,2021,30(8):1099-1114.DOI: 10.1111/exd.14414.
    [22] LvW,RenY,HouK,et al.Epigenetic modification mechanisms involved in keloid: current status and prospect[J].Clin Epigenetics,2020,12(1):183.DOI: 10.1186/s13148-020-00981-8.
    [23] HuangM,HuangJ,ZhengY,et al.Histone acetyltransferase inhibitors: an overview in synthesis, structure-activity relationship and molecular mechanism[J].Eur J Med Chem,2019,178:259-286.DOI: 10.1016/j.ejmech.2019.05.078.
    [24] SetoE,YoshidaM.Erasers of histone acetylation: the histone deacetylase enzymes[J].Cold Spring Harb Perspect Biol,2014,6(4):a018713.DOI: 10.1101/cshperspect.a018713.
    [25] 程希,徐慧雯,黄炜,等. 丁酸钠通过组蛋白丁酰化修饰改善糖尿病肾脏病炎症和纤维化[J]. 中华糖尿病杂志,2023,15(2):160-168. DOI: 10.3760/cma.j.cn115791-20220422-00177.
    [26] Fitzgerald O'ConnorEJ,BadshahII,AddaeLY,et al.Histone deacetylase 2 is upregulated in normal and keloid scars[J].J Invest Dermatol,2012,132(4):1293-1296.DOI: 10.1038/jid.2011.432.
    [27] TuT,HuangJ,LinM,et al.CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2[J].Int J Mol Med,2019,44(5):1789-1800.DOI: 10.3892/ijmm.2019.4348.
    [28] 仇克清基于定量修饰组学研究增生性瘢痕中差异赖氨酸乙酰化和琥珀酰化修饰南昌南昌大学医学部2023

    仇克清.基于定量修饰组学研究增生性瘢痕中差异赖氨酸乙酰化和琥珀酰化修饰[D].南昌:南昌大学医学部,2023.

    [29] JianX,QuL,WangY,et al.Trichostatin A-induced miR-30a-5p regulates apoptosis and proliferation of keloid fibroblasts via targeting BCL2[J].Mol Med Rep,2019,19(6):5251-5262.DOI: 10.3892/mmr.2019.10185.
    [30] LvD,XuZ,ChengP,et al.S-Nitrosylation-mediated coupling of DJ-1 with PTEN induces PI3K/AKT/mTOR pathway-dependent keloid formation[J/OL].Burns Trauma,2023,11:tkad024[2023-12-07].https://pubmed.ncbi.nlm.nih.gov/38116467/.DOI: 10.1093/burnst/tkad024.
    [31] IvanovGS,IvanovaT,KurashJ,et al.Methylation-acetylation interplay activates p53 in response to DNA damage[J].Mol Cell Biol,2007,27(19):6756-6769.DOI: 10.1128/MCB.00460-07.
    [32] Le CamL,LinaresLK,PaulC,et al.E4F1 is an atypical ubiquitin ligase that modulates p53 effector functions independently of degradation[J].Cell,2006,127(4):775-788.DOI: 10.1016/j.cell.2006.09.031.
    [33] LeiR,ZhangS,WangY,et al.Metformin inhibits epithelial-to-mesenchymal transition of keloid fibroblasts via the HIF-1α/PKM2 signaling pathway[J].Int J Med Sci,2019,16(7):960-966.DOI: 10.7150/ijms.32157.
    [34] ShangS,LiuJ,HuaF.Protein acylation: mechanisms, biological functions and therapeutic targets[J].Signal Transduct Target Ther,2022,7(1):396.DOI: 10.1038/s41392-022-01245-y.
    [35] McDonnellE,CrownSB,FoxDB,et al.Lipids reprogram metabolism to become a major carbon source for histone acetylation[J].Cell Rep,2016,17(6):1463-1472.DOI: 10.1016/j.celrep.2016.10.012.
    [36] CarrerA,TrefelyS,ZhaoS,et al.Acetyl-CoA metabolism supports multistep pancreatic tumorigenesis[J].Cancer Discov,2019,9(3):416-435.DOI: 10.1158/2159-8290.CD-18-0567.
    [37] NoeJT,RendonBE,GellerAE,et al.Lactate supports a metabolic-epigenetic link in macrophage polarization[J].Sci Adv,2021,7(46):eabi8602.DOI: 10.1126/sciadv.abi8602.
    [38] SeoudyWM,Mohy El DienSM,Abdel ReheemTA,et al.Macrophages of the M1 and M2 types play a role in keloids pathogenesis[J].Int Wound J,2023,20(1):38-45.DOI: 10.1111/iwj.13834.
    [39] WangJ,YangP,YuT,et al.Lactylation of PKM2 suppresses inflammatory metabolic adaptation in pro-inflammatory macrophages[J].Int J Biol Sci,2022,18(16):6210-6225.DOI: 10.7150/ijbs.75434.
    [40] FuY,YuJ,LiF,et al.Oncometabolites drive tumorigenesis by enhancing protein acylation: from chromosomal remodelling to nonhistone modification[J].J Exp Clin Cancer Res,2022,41(1):144.DOI: 10.1186/s13046-022-02338-w.
    [41] LiuX,ChenW,ZengQ,et al.Single-cell RNA-sequencing reveals lineage-specific regulatory changes of fibroblasts and vascular endothelial cells in keloids[J].J Invest Dermatol,2022,142(1):124-135.e11.DOI: 10.1016/j.jid.2021.06.010.
    [42] RhoH,TerryAR,ChronisC,et al.Hexokinase 2-mediated gene expression via histone lactylation is required for hepatic stellate cell activation and liver fibrosis[J].Cell Metab,2023,35(8):1406-1423.e8.DOI: 10.1016/j.cmet.2023.06.013.
    [43] DongZ,ZhuangQ,NingM,et al.Palmitic acid stimulates NLRP3 inflammasome activation through TLR4-NF-κB signal pathway in hepatic stellate cells[J].Ann Transl Med,2020,8(5):168.DOI: 10.21037/atm.2020.02.21.
    [44] GeJ,CuiH,XieN,et al.Glutaminolysis promotes collagen translation and stability via α-ketoglutarate-mediated mTOR activation and proline hydroxylation[J].Am J Respir Cell Mol Biol,2018,58(3):378-390.DOI: 10.1165/rcmb.2017-0238OC.
    [45] LiH,DixonEE,WuH,et al.Comprehensive single-cell transcriptional profiling defines shared and unique epithelial injury responses during kidney fibrosis[J].Cell Metab,2022,34(12):1977-1998.e9.DOI: 10.1016/j.cmet.2022.09.026.
    [46] 李珍玲,金哲虎,李莲花,等.瘢痕疙瘩的注射治疗现状及进展[J].临床皮肤科杂志,2023,52(12):758-761.DOI: 10.16761/j.cnki.1000-4963.2023.12.015.
    [47] LeeHJ,JangYJ.Recent understandings of biology, prophylaxis and treatment strategies for hypertrophic scars and keloids[J].Int J Mol Sci,2018,19(3):711.DOI: 10.3390/ijms19030711.
    [48] Abou-TalebDAE,BadaryDM.Intralesional verapamil in the treatment of keloids: a clinical, histopathological, and immunohistochemical study[J].J Cosmet Dermatol,2021,20(1):267-273.DOI: 10.1111/jocd.13476.
  • 加载中
计量
  • 文章访问数:  125
  • HTML全文浏览量:  60
  • PDF下载量:  13
  • 被引次数: 0
出版历程
  • 收稿日期:  2023-12-07
  • 网络出版日期:  2024-06-21

目录

    /

    返回文章
    返回