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有氧糖酵解在皮肤纤维化疾病中的作用研究进展

张丽霞 胡大海

张丽霞, 胡大海. 有氧糖酵解在皮肤纤维化疾病中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2024, 40(4): 389-394. DOI: 10.3760/cma.j.cn501225-20230712-00004.
引用本文: 张丽霞, 胡大海. 有氧糖酵解在皮肤纤维化疾病中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2024, 40(4): 389-394. DOI: 10.3760/cma.j.cn501225-20230712-00004.
Zhang LX,Hu DH.Research advances on the role of aerobic glycolysis in skin fibrosis diseases[J].Chin J Burns Wounds,2024,40(4):389-394.DOI: 10.3760/cma.j.cn501225-20230712-00004.
Citation: Zhang LX,Hu DH.Research advances on the role of aerobic glycolysis in skin fibrosis diseases[J].Chin J Burns Wounds,2024,40(4):389-394.DOI: 10.3760/cma.j.cn501225-20230712-00004.

有氧糖酵解在皮肤纤维化疾病中的作用研究进展

doi: 10.3760/cma.j.cn501225-20230712-00004
基金项目: 

国家自然科学基金面上项目 81372069, 81772071

空军军医大学第一附属医院学科助推计划军事医学基础研究专项 XJZT21J05

详细信息
    通讯作者:

    胡大海,Email:hudhai@fmmu.edu.cn

Research advances on the role of aerobic glycolysis in skin fibrosis diseases

Funds: 

General Program of National Natural Science Foundation of China 81372069, 81772071

The First Affiliated Hospital of Air Force Medical University Discipline Boosting Program for the Military Medical Basic Research Special Project XJZT21J05

More Information
  • 摘要: 皮肤纤维化疾病主要包括增生性瘢痕、瘢痕疙瘩及系统性硬化病等,其主要病理特点为成纤维细胞过度激活和细胞外基质异常沉积。近年来研究表明,有氧糖酵解与皮肤纤维化疾病的发生与发展密切相关,以有氧糖酵解为治疗靶点的药物为皮肤抗纤维化治疗提供了新的思路。该文就有氧糖酵解相关酶和产物在皮肤纤维化疾病发生与发展中的作用及靶向有氧糖酵解治疗皮肤纤维化疾病的药物进行综述。

     

  • 1  有氧糖酵解促成纤维细胞活化和增殖的机制

    注:α-SMA为α平滑肌肌动蛋白,PDK为丙酮酸脱氢酶激酶,PDH为丙酮酸脱氢酶,TCA为三羧酸循环,TGF-β为转化生长因子β

  • [1] WynnTA, RamalingamTR. Mechanisms of fibrosis: therapeutic translation for fibrotic disease[J]. Nat Med, 2012,18(7):1028-1040. DOI: 10.1038/nm.2807.
    [2] BairkdarM, RossidesM, WesterlindH, et al. Incidence and prevalence of systemic sclerosis globally: a comprehensive systematic review and meta-analysis[J]. Rheumatology (Oxford), 2021,60(7):3121-3133. DOI: 10.1093/rheumatology/keab190.
    [3] FinnertyCC, JeschkeMG, BranskiLK, et al. Hypertrophic scarring: the greatest unmet challenge after burn injury[J]. Lancet, 2016,388(10052):1427-1436. DOI: 10.1016/S0140-6736(16)31406-4.
    [4] HuangC, WuZ, DuY, et al. The epidemiology of keloids[M/OL]//Téot L, Mustoe TA, Middelkoop E, et al. Textbook on scar management: state of the art management and emerging technologies. Cham(CH): Springer, 2020: 29-35[2023-05-18]. http://link.springer.com/ 10.1007/978-3-030-44766-3_4. DOI: 10.1007/978-3-030-44766-3_4.
    [5] HendersonNC, RiederF, WynnTA. Fibrosis: from mechanisms to medicines[J]. Nature, 2020,587(7835):555-566. DOI: 10.1038/s41586-020-2938-9.
    [6] PlikusMV, WangXJ, SinhaS, et al. Fibroblasts: origins, definitions, and functions in health and disease[J]. Cell, 2021,184(15):3852-3872. DOI: 10.1016/j.cell.2021.06.024.
    [7] RodriguesM, KosaricN, BonhamCA, et al. Wound healing: a cellular perspective[J]. Physiol Rev, 2019, 99(1): 665-706. DOI: 10.1152/physrev.00067.2017.
    [8] BianXL, JiangHF, MengY, et al. Regulation of gene expression by glycolytic and gluconeogenic enzymes[J]. Trends Cell Biol, 2022,32(9):786-799. DOI: 10.1016/j.tcb.2022.02.003.
    [9] WarburgO, WindF, NegeleinE. The metabolism of tumors in the body[J]. J Gen Physiol, 1927, 8(6): 519-530. DOI: 10.1085/jgp.8.6.519.
    [10] XieN, TanZ, BanerjeeS, et al. Glycolytic reprogramming in myofibroblast differentiation and lung fibrosis[J]. Am J Respir Crit Care Med, 2015, 192(12): 1462-1474. DOI: 10.1164/rccm.201504-0780OC.
    [11] ChenZT, GaoQY, WuMX, et al. Glycolysis inhibition alleviates cardiac fibrosis after myocardial infarction by suppressing cardiac fibroblast activation[J]. Front Cardiovasc Med, 2021, 8: 701745. DOI: 10.3389/fcvm.2021.701745.
    [12] HuangT, LiYQX, ZhouMY, et al. Focal adhesion kinase-related non-kinase ameliorates liver fibrosis by inhibiting aerobic glycolysis via the FAK/Ras/c-myc/ENO1 pathway[J]. World J Gastroenterol, 2022,28(1):123-139. DOI: 10.3748/wjg.v28.i1.123.
    [13] ZhaoX, PsarianosP, GhoraieLS, et al. Metabolic regulation of dermal fibroblasts contributes to skin extracellular matrix homeostasis and fibrosis[J]. Nat Metab, 2019,1(1):147-157. DOI: 10.1038/s42255-018-0008-5.
    [14] OzawaT, OkamuraT, HaradaT, et al. Accumulation of glucose in keloids with FDG-PET[J]. Ann Nucl Med, 2006,20(1):41-44. DOI: 10.1007/BF02985589.
    [15] OkunoR, ItoY, EidN, et al. Upregulation of autophagy and glycolysis markers in keloid hypoxic-zone fibroblasts: morphological characteristics and implications[J]. Histol Histopathol, 2018,33(10):1075-1087. DOI: 10.14670/HH-18-005.
    [16] SitKH, LauYK, AwSE. Differential oxygen sensitivities in G6PDH activities of cultured keloid and normal skin dermis single cells[J]. J Dermatol, 1991,18(10):572-579. DOI: 10.1111/j.1346-8138.1991.tb03135.x.
    [17] 苏治国,范金财,刘立强, 等. 瘢痕疙瘩成纤维细胞中Warburg效应的研究[J]. 中华整形外科杂志,2020,36(10):1100-1105. DOI: 10.3760/cma.j.cn114453-20200220-00064.
    [18] 杨怡圆, 周仁鹏, 候家琳, 等. M2型丙酮酸激酶对瘢痕疙瘩成纤维细胞功能的影响[J].组织工程与重建外科杂志,2020,16(5):351-358. DOI: 10.3969/j.issn.1673-0364.2020.05.002.
    [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] AndreucciE, MargheriF, PeppicelliS, et al. Glycolysis-derived acidic microenvironment as a driver of endothelial dysfunction in systemic sclerosis[J]. Rheumatology (Oxford), 2021,60(10):4508-4519. DOI: 10.1093/rheumatology/keab022.
    [21] VincentAS, PhanTT, MukhopadhyayA, et al. Human skin keloid fibroblasts display bioenergetics of cancer cells[J]. J Invest Dermatol, 2008,128(3):702-709. DOI: 10.1038/sj.jid.5701107.
    [22] ShenY, JiangL, WenP, et al. Tubule-derived lactate is required for fibroblast activation in acute kidney injury[J]. Am J Physiol Renal Physiol, 2020,318(3):F689-F701. DOI: 10.1152/ajprenal.00229.2019.
    [23] FrangogiannisN. Transforming growth factor-β in tissue fibrosis[J]. J Exp Med, 2020,217(3):e20190103. DOI: 10.1084/jem.20190103.
    [24] ShiML, ZhuJH, WangR, et al. Latent TGF-β structure and activation[J]. Nature, 2011,474(7351):343-349. DOI: 10.1038/nature10152.
    [25] KottmannRM, KulkarniAA, SmolnyckiKA, et al. Lactic acid is elevated in idiopathic pulmonary fibrosis and induces myofibroblast differentiation via pH-dependent activation of transforming growth factor-β[J]. Am J Respir Crit Care Med, 2012,186(8):740-751. DOI: 10.1164/rccm.201201-0084OC.
    [26] LiuWH, WangY, BoziLHM, et al. Lactate regulates cell cycle by remodelling the anaphase promoting complex[J]. Nature, 2023, 616(7958): 790-797. DOI: 10.1038/s41586-023-05939-3.
    [27] IyerNV, KotchLE, AganiF, et al. Cellular and developmental control of O 2 homeostasis by hypoxia-inducible factor 1α[J]. Genes Dev, 1998, 12(2): 149-162. DOI: 10.1101/gad.12.2.149.
    [28] KimJW, TchernyshyovI, SemenzaGL, et al. HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia[J]. Cell Metab, 2006,3(3):177-185. DOI: 10.1016/j.cmet.2006.02.002.
    [29] NagaoA, KobayashiM, KoyasuS, et al. HIF-1-dependent reprogramming of glucose metabolic pathway of cancer cells and its therapeutic significance[J]. Int J Mol Sci, 2019, 20(2): 238. DOI: 10.3390/ijms20020238.
    [30] WangQF, WangP, QinZL, et al. Altered glucose metabolism and cell function in keloid fibroblasts under hypoxia[J]. Redox Biol, 2021,38:101815. DOI: 10.1016/j.redox.2020.101815.
    [31] LiJY, YinYL, ZhangEY, et al. Peptide deregulated in hypertrophic scar-1 alleviates hypertrophic scar fibrosis by targeting focal adhesion kinase and pyruvate kinase M2 and remodeling the metabolic landscape[J]. Int J Biol Macromol, 2023,235:123809. DOI: 10.1016/j.ijbiomac.2023.123809.
    [32] AlquraishiM, PuckettDL, AlaniDS, et al. Pyruvate kinase M2: a simple molecule with complex functions[J]. Free Radic Biol Med, 2019,143:176-192. DOI: 10.1016/j.freeradbiomed.2019.08.007.
    [33] ZhengDD, JiangYC, QuC, et al. Pyruvate kinase M2 tetramerization protects against hepatic stellate cell activation and liver fibrosis[J]. Am J Pathol, 2020, 190(11): 2267-2281. DOI: 10.1016/j.ajpath.2020.08.002.
    [34] GaoJ, WeiT, HuangCL, et al. Sirtuin 3 governs autophagy-dependent glycolysis during Angiotensin Ⅱ-induced endothelial-to-mesenchymal transition[J]. FASEB J, 2020,34(12):16645-16661. DOI: 10.1096/fj.202001494R.
    [35] GaoSY, LiXH, JiangQY, et al. PKM2 promotes pulmonary fibrosis by stabilizing TGF-β 1receptor I and enhancing TGF-β 1 signaling[J]. Sci Adv, 2022,8(38):eabo0987. DOI: 10.1126/sciadv.abo0987.
    [36] VinaikR, BarayanD, AugerC, et al. Regulation of glycolysis and the Warburg effect in wound healing[J]. JCI Insight, 2020,5(17):e138949. DOI: 10.1172/jci.insight.138949.
    [37] ZhouMY, ChengML, HuangT, et al. Transforming growth factor beta-1 upregulates glucose transporter 1 and glycolysis through canonical and noncanonical pathways in hepatic stellate cells[J]. World J Gastroenterol, 2021,27(40):6908-6926. DOI: 10.3748/wjg.v27.i40.6908.
    [38] WangP, WangQF, YangX, et al. Targeting the glycolytic enzyme PGK1 to inhibit the Warburg effect: a new strategy for keloid therapy[J]. Plastic Reconstr Surg, 2023, 151(6): 970e-980e. DOI: 10.1097/PRS.0000000000010137.
    [39] MeiSY, XuQY, HuY, et al. Integrin β3-PKM2 pathway-mediated aerobic glycolysis contributes to mechanical ventilation-induced pulmonary fibrosis[J]. Theranostics, 2022,12(14):6057-6068. DOI: 10.7150/thno.72328.
    [40] LiQ, QinZL, NieFF, 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.
    [41] SchrufE, SchroederV, KuttruffCA, et al. Human lung fibroblast-to-myofibroblast transformation is not driven by an LDH5-dependent metabolic shift towards aerobic glycolysis[J]. Respir Res, 2019,20(1):87. DOI: 10.1186/s12931-019-1058-2.
    [42] WangFX, JiaY, LiMM, et al. Blockade of glycolysis-dependent contraction by oroxylin a via inhibition of lactate dehydrogenase-a in hepatic stellate cells[J]. Cell Commun Signal, 2019,17(1):11. DOI: 10.1186/s12964-019-0324-8.
    [43] LiuYZ, BaiF, LiuN, et al. Metformin improves lipid metabolism and reverses the Warburg effect in a canine model of chronic atrial fibrillation[J]. BMC Cardiovasc Disord, 2020,20(1):50. DOI: 10.1186/s12872-020-01359-7.
    [44] TangCJ, XuJ, YeHY, et al. Metformin prevents PFKFB3-related aerobic glycolysis from enhancing collagen synthesis in lung fibroblasts by regulating AMPK/mTOR pathway[J]. Exp Ther Med, 2021,21(6):581. DOI: 10.3892/etm.2021.10013.
    [45] YuHL, ZhuJB, ChangLY, et al. 3-Bromopyruvate decreased kidney fibrosis and fibroblast activation by suppressing aerobic glycolysis in unilateral ureteral obstruction mice model[J]. Life Sci, 2021,272:119206. DOI: 10.1016/j.lfs.2021.119206.
    [46] WangW, ZhangY, HuangWH, et al. Alamandine/MrgD axis prevents TGF-β 1-mediated fibroblast activation via regulation of aerobic glycolysis and mitophagy[J]. J Transl Med, 2023,21(1):24. DOI: 10.1186/s12967-022-03837-2.
    [47] FanN, ZhangXY, ZhaoW, et al. Covalent inhibition of pyruvate kinase M2 reprograms metabolic and inflammatory pathways in hepatic macrophages against non-alcoholic fatty liver disease[J]. Int J Biol Sci, 2022, 18(14): 5260-5275. DOI: 10.7150/ijbs.73890.
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  • 收稿日期:  2023-07-12

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