Email Alerts
RSS
Volume 39 Issue 2
Feb.  2023
Turn off MathJax
Article Contents
Article Navigation >  CHINESE JOURNAL OF BURNS AND WOUNDS  > 2023  >  39(2): 106-113
He WF,Yan LF.The regulatory role and related mechanisms of macrophages in wound healing[J].Chin J Burns Wounds,2023,39(2):106-113.DOI: 10.3760/cma.j.cn501225-20230110-00010.
Citation: He WF,Yan LF.The regulatory role and related mechanisms of macrophages in wound healing[J].Chin J Burns Wounds,2023,39(2):106-113.DOI: 10.3760/cma.j.cn501225-20230110-00010.
shu

The regulatory role and related mechanisms of macrophages in wound healing

doi: 10.3760/cma.j.cn501225-20230110-00010

  • State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burn Research, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing Key Laboratory for Disease Proteomics, Chongqing 400038, China

Funds:

General Program of National Natural Science Foundation of China 31872742, 82172232

Military Medical Science and Technology Youth Training Program 20QNPY024

Special Project for Enhancing Science and Technology Innovation Ability of Army Medical University 2019XQY12

More Information
    Abstract
  • Wound healing is a complex process under precise regulation, including multiple stages such as inflammation, anti-inflammatory, and regeneration. Macrophages play an important regulatory role in the differentiated process of wound healing due to their obvious plasticity. If macrophages fail to express specific functions in a timely manner, it will affect the healing function of tissues and lead to pathological tissue healing. Therefore, it is of great significance to understand the different functions of different types of macrophages and to regulate them specifically in different stages of wound healing to promote the healing and regeneration of wound tissue. In this paper, we illustrate the different functions of macrophages in the wound and their basic mechanisms, according to the basic process of wound healing, and emphasize the strategies of macrophage regulation that may be applied to clinical treatment in the future.

     

    • FullText(HTML)
  • loading
    • References(53)
  • [1]
    BoniakowskiAE, KimballAS, JacobsBN,et al. Macrophage-mediated inflammation in normal and diabetic wound healing[J].J Immunol,2017,199(1):17-24. DOI: 10.4049/jimmunol.1700223.
    [2]
    NobsSP, KopfM. Tissue-resident macrophages: guardians of organ homeostasis[J].Trends Immunol,2021,42(6):495-507. DOI: 10.1016/j.it.2021.04.007.
    [3]
    ChakarovS, LimHY, TanL,et al. Two distinct interstitial macrophage populations coexist across tissues in specific subtissular niches[J].Science,2019,363(6432):eaau0964.DOI: 10.1126/science.aau0964.
    [4]
    YapJ, IreiJ, Lozano-GeronaJ,et al. Macrophages in cardiac remodelling after myocardial infarction[J].Nat Rev Cardiol,2023.DOI: 10.1038/s41569-022-00823-5.
    [5]
    WynnTA and VannellaKM. Macrophages in tissue repair, regeneration, and fibrosis[J].Immunity,2016,44(3):450-462. DOI: 10.1016/j.immuni.2016.02.015.
    [6]
    FunesSC, RiosM, Escobar-VeraJ,et al. Implications of macrophage polarization in autoimmunity[J].Immunology,2018,154(2):186-195. DOI: 10.1111/imm.12910.
    [7]
    ZindelJ, KubesP. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation[J].Annu Rev Pathol,2020,15:493-518. DOI: 10.1146/annurev-pathmechdis-012419-032847.
    [8]
    BakogiannisC, SachseM, StamatelopoulosK,et al. Platelet-derived chemokines in inflammation and atherosclerosis[J].Cytokine,2019,122:154157. DOI: 10.1016/j.cyto.2017.09.013.
    [9]
    HassanshahiA, MoradzadM, GhalamkariS,et al. Macrophage-mediated inflammation in skin wound healing[J].Cells,2022,11(19) :2953.DOI: 10.3390/cells11192953.
    [10]
    FountainA, InpanathanS, AlvesP,et al. Phagosome maturation in macrophages: eat, digest, adapt, and repeat[J].Adv Biol Regul,2021,82:100832. DOI: 10.1016/j.jbior.2021.100832.
    [11]
    GengJ, ShiY, ZhangJ,et al. TLR4 signalling via Piezo1 engages and enhances the macrophage mediated host response during bacterial infection[J].Nat Commun,2021,12(1):3519. DOI: 10.1038/s41467-021-23683-y.
    [12]
    XuX, PiaoHN, AosaiF,et al. Arctigenin protects against depression by inhibiting microglial activation and neuroinflammation via HMGB1/TLR4/ NF-κB and TNF-α/TNFR1/ NF-κB pathways[J].Br J Pharmacol,2020,177(22):5224-5245. DOI: 10.1111/bph.15261.
    [13]
    ZumerleS, CalìB, MunariF,et al. Intercellular calcium signaling induced by ATP potentiates macrophage phagocytosis[J].Cell Rep,2019,27(1):1-10.e4. DOI: 10.1016/j.celrep.2019.03.011.
    [14]
    ChenW, LiuY, ChenJ,et al. The Notch signaling pathway regulates macrophage polarization in liver diseases[J].Int Immunopharmacol,2021,99:107938. DOI: 10.1016/j.intimp.2021.107938.
    [15]
    YunnaC, MengruH, LeiW,et al. Macrophage M1/M2 polarization[J].Eur J Pharmacol,2020,877:173090. DOI: 10.1016/j.ejphar.2020.173090.
    [16]
    McCubbreyAL, McManusSA, McClendonJD,et al. Polyamine import and accumulation causes immunomodulation in macrophages engulfing apoptotic cells[J].Cell Rep,2022,38(2):110222. DOI: 10.1016/j.celrep.2021.110222.
    [17]
    Greenlee-WackerMC. Clearance of apoptotic neutrophils and resolution of inflammation[J].Immunol Rev,2016,273(1):357-370. DOI: 10.1111/imr.12453.
    [18]
    LaskinDL,MalaviyaR, LaskinJD. Role of macrophages in acute lung injury and chronic fibrosis induced by pulmonary toxicants[J].Toxicol Sci,2019,168(2):287-301. DOI: 10.1093/toxsci/kfy309.
    [19]
    WuH, ZhengJ, XuS,et al. Mer regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following traumatic brain injury[J].J Neuroinflammation,2021,18(1):2. DOI: 10.1186/s12974-020-02041-7.
    [20]
    ShouvalDS, BiswasA, GoettelJA,et al. Interleukin-10 receptor signaling in innate immune cells regulates mucosal immune tolerance and anti-inflammatory macrophage function[J].Immunity,2014,40(5):706-719. DOI: 10.1016/j.immuni.2014.03.011.
    [21]
    ArnoldL, HenryA, PoronF,et al. Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis[J].J Exp Med,2007,204(5):1057-1069. DOI: 10.1084/jem.20070075.
    [22]
    BouhlelMA, DerudasB, RigamontiE,et al. PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties[J].Cell Metab,2007,6(2):137-143. DOI: 10.1016/j.cmet.2007.06.010.
    [23]
    BaoL, DouG, TianR,et al. Engineered neutrophil apoptotic bodies ameliorate myocardial infarction by promoting macrophage efferocytosis and inflammation resolution[J].Bioact Mater,2022,9:183-197. DOI: 10.1016/j.bioactmat.2021.08.008.
    [24]
    HilgendorfI, GerhardtLM, TanTC,et al. Ly-6Chigh monocytes depend on Nr4a1 to balance both inflammatory and reparative phases in the infarcted myocardium[J].Circ Res,2014,114(10):1611-1622. DOI: 10.1161/circresaha.114.303204.
    [25]
    WangX, CaoQ, YuL,et al. Epigenetic regulation of macrophage polarization and inflammation by DNA methylation in obesity[J].JCI Insight,2016,1(19):e87748. DOI: 10.1172/jci.insight.87748.
    [26]
    MullicanSE, GaddisCA, AlenghatT,et al. Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation[J].Genes Dev,2011,25(23):2480-2488. DOI: 10.1101/gad.175950.111.
    [27]
    CurtaleG,RubinoM, LocatiM. MicroRNAs as molecular switches in macrophage activation[J].Front Immunol,2019,10:799. DOI: 10.3389/fimmu.2019.00799.
    [28]
    BernshteinB, CuratoC, IoannouM,et al. IL-23-producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven proinflammatory epithelial cell response[J].Sci Immunol,2019,4(36):eaau6571. DOI: 10.1126/sciimmunol.aau6571.
    [29]
    JungM, MaY, IyerRP,et al. IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation[J].Basic Res Cardiol,2017,112(3):33. DOI: 10.1007/s00395-017-0622-5.
    [30]
    De NardoD, LabzinLI, KonoH,et al. High-density lipoprotein mediates anti-inflammatory reprogramming of macrophages via the transcriptional regulator ATF3[J].Nat Immunol,2014,15(2):152-160. DOI: 10.1038/ni.2784.
    [31]
    WestphalenK, GusarovaGA, IslamMN,et al. Sessile alveolar macrophages communicate with alveolar epithelium to modulate immunity[J].Nature,2014,506(7489):503-506. DOI: 10.1038/nature12902.
    [32]
    JeongH, YoonH, LeeY,et al. SOCS3 attenuates dexamethasone-induced M2 polarization by down-regulation of GILZ via ROS- and p38 MAPK-dependent pathways[J].Immune Netw,2022,22(4):e33. DOI: 10.4110/in.2022.22.e33.
    [33]
    KimH, WangSY, KwakG,et al. Exosome-guided phenotypic switch of M1 to M2 macrophages for cutaneous wound healing[J].Adv Sci (Weinh),2019,6(20):1900513. DOI: 10.1002/advs.201900513.
    [34]
    WillenborgS, LucasT, van LooG,et al. CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair[J].Blood,2012,120(3):613-625. DOI: 10.1182/blood-2012-01-403386.
    [35]
    MantsoungaCS, LeeC, NeversonJ,et al. Macrophage IL-1β promotes arteriogenesis by autocrine STAT3- and NF-κB-mediated transcription of pro-angiogenic VEGF-A[J].Cell Rep,2022,38(5):110309. DOI: 10.1016/j.celrep.2022.110309.
    [36]
    GantaVC, ChoiM, FarberCR,et al. Antiangiogenic VEGF(165)b regulates macrophage polarization via S100A8/S100A9 in peripheral artery disease[J].Circulation,2019,139(2):226-242. DOI: 10.1161/circulationaha.118.034165.
    [37]
    XiaoH, ZhaoX, LiS,et al. Risk factors for subretinal fibrosis after anti-VEGF treatment of myopic choroidal neovascularisation[J].Br J Ophthalmol,2021,105(1):103-108. DOI: 10.1136/bjophthalmol-2019-315763.
    [38]
    PakshirP, HinzB. The big five in fibrosis: macrophages, myofibroblasts, matrix, mechanics, and miscommunication[J].Matrix Biol,2018,68-69,81-93. DOI: 10.1016/j.matbio.2018.01.019.
    [39]
    BorthwickLA, BarronL, HartKM,et al. Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis[J].Mucosal Immunol,2016,9(1):38-55. DOI: 10.1038/mi.2015.34.
    [40]
    MengXM, WangS, HuangXR,et al. Inflammatory macrophages can transdifferentiate into myofibroblasts during renal fibrosis[J].Cell Death Dis,2016,7(12):e2495. DOI: 10.1038/cddis.2016.402.
    [41]
    TangPC, ChungJY, XueVW,et al. Smad3 promotes cancer-associated fibroblasts generation via macrophage-myofibroblast transition[J].Adv Sci (Weinh),2022,9(1):e2101235. DOI: 10.1002/advs.202101235.
    [42]
    ShookBA, WaskoRR, Rivera-GonzalezGC,et al. Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair[J].Science,2018,362(6417):eaar2971. DOI: 10.1126/science.aar2971.
    [43]
    AbeH, TakedaN, IsagawaT,et al. Macrophage hypoxia signaling regulates cardiac fibrosis via Oncostatin M[J].Nat Commun,2019,10(1):2824. DOI: 10.1038/s41467-019-10859-w.
    [44]
    StutchfieldBM, AntoineDJ, MackinnonAC,et al. CSF1 restores innate immunity after liver injury in mice and serum levels indicate outcomes of patients with acute liver failure[J].Gastroenterology,2015,149(7):1896-1909.e14. DOI: 10.1053/j.gastro.2015.08.053.
    [45]
    WuDC, KolliparaR, CarterMJ,et al. A novel macrophage-activating gel improves healing and skin quality after CO2 laser resurfacing of the chest[J].Dermatol Surg,2022,48(12):1312-1316. DOI: 10.1097/dss.0000000000003622.
    [46]
    SchmittH, UlmschneiderJ, BillmeierU,et al. The TLR9 agonist cobitolimod induces IL10-producing wound healing macrophages and regulatory T cells in ulcerative colitis[J].J Crohns Colitis,2020,14(4):508-524. DOI: 10.1093/ecco-jcc/jjz170.
    [47]
    李晓亮, 谢江帆, 叶向阳, 等. 非编码RNA调控糖尿病创面愈合机制的研究进展[J]. 中华烧伤与创面修复杂志, 2023, 39(2): 184-189. DOI: 10.3760/cma.j.cn501225-20221101-00477.
    [48]
    ZhouLS, ZhaoGL, LiuQ,et al. Silencing collapsin response mediator protein-2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction model[J].J Inflamm (Lond),2015,12:11. DOI: 10.1186/s12950-015-0053-8.
    [49]
    WuX, HeW, MuX,et al. Macrophage polarization in diabetic wound healing[J/OL].Burns Trauma,2022,10:tkac051[2023-01-10].https://pubmed.ncbi.nlm.nih.gov/34089902/.DOI: 10.1093/burnst/tkac051.
    [50]
    LiS, YangP, DingX,et al. Puerarin improves diabetic wound healing via regulation of macrophage M2 polarization phenotype[J/OL].Burns Trauma,2022,10:tkac046[2023-01-10]. https://pubmed.ncbi.nlm.nih.gov/36568527/.DOI: 10.1093/burnst/tkac046.
    [51]
    HuangYY, LinCW, ChengNC,et al. Effect of a novel macrophage-regulating drug on wound healing in patients with diabetic foot ulcers: a randomized clinical trial[J].JAMA Netw Open,2021,4(9):e2122607. DOI: 10.1001/jamanetworkopen.2021.22607.
    [52]
    LopesT, AlmeidaGG, SouzaIA,et al. High-density- immune-complex regulatory macrophages promote recovery of erxperimental colitis in mice[J].Inflammation,2021,44(3):1069-1082. DOI: 10.1007/s10753-020-01403-w.
    [53]
    MuR, ZhangZ, HanC,et al. Tumor-associated macrophages-educated reparative macrophages promote diabetic wound healing[J].EMBO Mol Med,2023,15(2):e16671. DOI: 10.15252/emmm.202216671.
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(1)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (2624) PDF downloads(89) Cited by()
    Proportional views
    Related

    Copyright © Chinese Journal of Burns京ICP备07035254号-14

    E-mail：shaoshangzazhi@163.com

    Website：https://zhsszz.xml-journal.net/

    Supported by: Beijing Renhe Information Technology Co. Ltd    

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return