Association between glycolysis and mitochondrial dysfunction and its potential value in liver diseases

Gengjie YAN; Yong LIN; Huiji SU; Hanxiao CHEN; Shaoqun BAN; Ailing WEI; Dewen MAO; Fuli LONG

doi:10.3969/j.issn.1001-5256.2022.08.042

Volume 38 Issue 8

Aug. 2022

Turn off MathJax

Article Contents

Abstract

References

Article Navigation > Journal of Clinical Hepatology > 2022 > 38(8): 1931-1936

PDF( 2522 KB)

Association between glycolysis and mitochondrial dysfunction and its potential value in liver diseases

DOI: 10.3969/j.issn.1001-5256.2022.08.042

1.
Graduate School of Guangxi University of Chinese Medicine, Nanning 530200, China
2.
Second Ward of Hepatology, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China

Research funding:

National Natural Science Foundation of China (81960841);

National Science and Technology Major Project (2018ZX10725505-001-011);

Guangxi Science and Technology Project (2020GXNSFAA297098);

Guangxi University of Traditional Chinese Medicine Graduate Innovation Project (YCXJ2021034)

More Information

Corresponding author: LONG Fuli, longfuli005@163.com(ORCID: 0000-0003-1196-2697)
Received Date: 2022-04-18
Accepted Date: 2022-05-29
Published Date: 2022-08-20

Abstract

Abstract

Glycolysis plays an important role in the development and progression of liver diseases and shows varying degrees of enhancement in different liver diseases, and it is closely associated with mitochondrial dysfunction (oxidative phosphorylation deficiency and reactive oxygen species production), which helps to fill energy production deficiency caused by impaired oxidative phosphorylation. Therefore, it might be possible to search for potential new therapies for liver diseases through targeted regulation of the key factors in aerobic glycolysis, such as hexokinase 2, pyruvate kinase M2, and other regulatory pathways. From the perspective of the association between glycolysis and liver diseases, this article elaborates on the therapeutic significance and potential value of glycolysis in liver diseases, in order to provide new ideas for the diagnosis and treatment of liver diseases.
- Liver Diseases,
- Glycolysis,
- Mitochondria

FullText(HTML)

References(45)

References

[1]	AUGER C, ALHASAWI A, CONTAVADOO M, et al. Dysfunctional mitochondrial bioenergetics and the pathogenesis of hepatic disorders[J]. Front Cell Dev Biol, 2015, 3: 40. DOI: 10.3389/fcell.2015.00040.
[2]	WALLACE DC, FAN W, PROCACCIO V. Mitochondrial energetics and therapeutics[J]. Annu Rev Pathol, 2010, 5: 297-348. DOI: 10.1146/annurev.pathol.4.110807.092314.
[3]	NISHIKAWA T, BELLANCE N, DAMM A, et al. A switch in the source of ATP production and a loss in capacity to perform glycolysis are hallmarks of hepatocyte failure in advance liver disease[J]. J Hepatol, 2014, 60(6): 1203-1211. DOI: 10.1016/j.jhep.2014.02.014.
[4]	GO Y, JEONG JY, JEOUNG NH, et al. Inhibition of pyruvate dehydrogenase kinase 2 protects against hepatic steatosis through modulation of tricarboxylic acid cycle anaplerosis and ketogenesis[J]. Diabetes, 2016, 65(10): 2876-2887. DOI: 10.2337/db16-0223.
[5]	ZHANG M, ZHAO Y, LI Z, et al. Pyruvate dehydrogenase kinase 4 mediates lipogenesis and contributes to the pathogenesis of nonalcoholic steatohepatitis[J]. Biochem Biophys Res Commun, 2018, 495(1): 582-586. DOI: 10.1016/j.bbrc.2017.11.054.
[6]	SHIRAI T, NAZAREWICZ RR, WALLIS BB, et al. The glycolytic enzyme PKM2 bridges metabolic and inflammatory dysfunction in coronary artery disease[J]. J Exp Med, 2016, 213(3): 337-354. DOI: 10.1084/jem.20150900.
[7]	MIDDLETON P, VERGIS N. Mitochondrial dysfunction and liver disease: role, relevance, and potential for therapeutic modulation[J]. Therap Adv Gastroenterol, 2021, 14: 17562848211031394. DOI: 10.1177/17562848211031394.
[8]	GABBIA D, CANNELLA L, DE MARTIN S. The role of oxidative stress in NAFLD-NASH-HCC transition-focus on NADPH oxidases[J]. Biomedicines, 2021, 9(6): 687. DOI: 10.3390/biomedicines9060687.
[9]	LEE N, CARELLA MA, PAPA S, et al. High expression of glycolytic genes in cirrhosis correlates with the risk of developing liver cancer[J]. Front Cell Dev Biol, 2018, 6: 138. DOI: 10.3389/fcell.2018.00138.
[10]	LI S, LI J, DAI W, et al. Genistein suppresses aerobic glycolysis and induces hepatocellular carcinoma cell death[J]. Br J Cancer, 2017, 117(10): 1518-1528. DOI: 10.1038/bjc.2017.323.
[11]	YE JH, CHAO J, CHANG ML, et al. Pentoxifylline ameliorates non-alcoholic fatty liver disease in hyperglycaemic and dyslipidaemic mice by upregulating fatty acid β-oxidation[J]. Sci Rep, 2016, 6: 33102. DOI: 10.1038/srep33102.
[12]	SHANG RZ, QU SB, WANG DS. Reprogramming of glucose metabolism in hepatocellular carcinoma: Progress and prospects[J]. World J Gastroenterol, 2016, 22(45): 9933-9943. DOI: 10.3748/wjg.v22.i45.9933.
[13]	LUNT SY, VANDER HEIDEN MG. Aerobic glycolysis: meeting the metabolic requirements of cell proliferation[J]. Annu Rev Cell Dev Biol, 2011, 27: 441-464. DOI: 10.1146/annurev-cellbio-092910-154237.
[14]	SCIACOVELLI M, GAUDE E, HILVO M, et al. The metabolic alterations of cancer cells[J]. Methods Enzymol, 2014, 542: 1-23. DOI: 10.1016/B978-0-12-416618-9.00001-7.
[15]	LIU J, JIANG S, ZHAO Y, et al. Geranylgeranyl diphosphate synthase (GGPPS) regulates non-alcoholic fatty liver disease (NAFLD)-fibrosis progression by determining hepatic glucose/fatty acid preference under high-fat diet conditions[J]. J Pathol, 2018, 246(3): 277-288. DOI: 10.1002/path.5131.
[16]	KORS L, RAMPANELLI E, STOKMAN G, et al. Deletion of NLRX1 increases fatty acid metabolism and prevents diet-induced hepatic steatosis and metabolic syndrome[J]. Biochim Biophys Acta Mol Basis Dis, 2018, 1864(5 Pt A): 1883-1895. DOI: 10.1016/j.bbadis.2018.03.003.
[17]	SHANNON CE, RAGAVAN M, PALAVICINI JP, et al. Insulin resistance is mechanistically linked to hepatic mitochondrial remodeling in non-alcoholic fatty liver disease[J]. Mol Metab, 2021, 45: 101154. DOI: 10.1016/j.molmet.2020.101154.
[18]	WANG T, CHEN K, YAO W, et al. Acetylation of lactate dehydrogenase B drives NAFLD progression by impairing lactate clearance[J]. J Hepatol, 2021, 74(5): 1038-1052. DOI: 10.1016/j.jhep.2020.11.028.
[19]	SHIMADA K, CROTHER TR, KARLIN J, et al. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis[J]. Immunity, 2012, 36(3): 401-414. DOI: 10.1016/j.immuni.2012.01.009.
[20]	XU F, GUO M, HUANG W, et al. Annexin A5 regulates hepatic macrophage polarization via directly targeting PKM2 and ameliorates NASH[J]. Redox Biol, 2020, 36: 101634. DOI: 10.1016/j.redox.2020.101634.
[21]	SUN M, KISSELEVA T. Reversibility of liver fibrosis[J]. Clin Res Hepatol Gastroenterol, 2015, 39(Suppl 1): S60-S63. DOI: 10.1016/j.clinre.2015.06.015.
[22]	WANG F, JIA Y, LI M, 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.
[23]	WAN L, XIA T, DU Y, et al. Exosomes from activated hepatic stellate cells contain GLUT1 and PKM2: a role for exosomes in metabolic switch of liver nonparenchymal cells[J]. FASEB J, 2019, 33(7): 8530-8542. DOI: 10.1096/fj.201802675R.
[24]	HUANG T, LI YQ, ZHOU MY, 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.
[25]	RAO J, WANG H, NI M, et al. FSTL1 promotes liver fibrosis by reprogramming macrophage function through modulating the intracellular function of PKM2[J]. Gut, 2022. DOI: 10.1136/gutjnl-2021-325150.[Online ahead of print]
[26]	ZHENG D, JIANG Y, QU C, 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.
[27]	ZHOU MY, CHENG ML, HUANG T, 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.
[28]	BAN D, HUA S, ZHANG W, et al. Costunolide reduces glycolysis-associated activation of hepatic stellate cells via inhibition of hexokinase-2[J]. Cell Mol Biol Lett, 2019, 24: 52. DOI: 10.1186/s11658-019-0179-4.
[29]	MATHUPALA SP, KO YH, PEDERSEN PL. Hexokinase-2 bound to mitochondria: cancer's stygian link to the "Warburg Effect" and a pivotal target for effective therapy[J]. Semin Cancer Biol, 2009, 19(1): 17-24. DOI: 10.1016/j.semcancer.2008.11.006.
[30]	VAUPEL P, SCHMIDBERGER H, MAYER A. The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression[J]. Int J Radiat Biol, 2019, 95(7): 912-919. DOI: 10.1080/09553002.2019.1589653.
[31]	DEWAAL D, NOGUEIRA V, TERRY AR, et al. Hexokinase-2 depletion inhibits glycolysis and induces oxidative phosphorylation in hepatocellular carcinoma and sensitizes to metformin[J]. Nat Commun, 2018, 9(1): 446. DOI: 10.1038/s41467-017-02733-4.
[32]	MATHUPALA SP, KO YH, PEDERSEN PL. Hexokinase-2 bound to mitochondria: cancer's stygian link to the "Warburg Effect" and a pivotal target for effective therapy[J]. Semin Cancer Biol, 2009, 19(1): 17-24. DOI: 10.1016/j.semcancer.2008.11.006.
[33]	KANAI S, SHIMADA T, NARITA T, et al. Phosphofructokinase-1 subunit composition and activity in the skeletal muscle, liver, and brain of dogs[J]. J Vet Med Sci, 2019, 81(5): 712-716. DOI: 10.1292/jvms.19-0049.
[34]	BARTRONS R, RODRÍGUEZ-GARCÍA A, SIMON-MOLAS H, et al. The potential utility of PFKFB3 as a therapeutic target[J]. Expert Opin Ther Targets, 2018, 22(8): 659-674. DOI: 10.1080/14728222.2018.1498082.
[35]	LI S, DAI W, MO W, et al. By inhibiting PFKFB3, aspirin overcomes sorafenib resistance in hepatocellular carcinoma[J]. Int J Cancer, 2017, 141(12): 2571-2584. DOI: 10.1002/ijc.31022.
[36]	van NIEKERK G, ENGELBRECHT AM. Role of PKM2 in directing the metabolic fate of glucose in cancer: a potential therapeutic target[J]. Cell Oncol (Dordr), 2018, 41(4): 343-351. DOI: 10.1007/s13402-018-0383-7.
[37]	AZOITEI N, BECHER A, STEINESTEL K, et al. PKM2 promotes tumor angiogenesis by regulating HIF-1α through NF-κB activation[J]. Mol Cancer, 2016, 15: 3. DOI: 10.1186/s12943-015-0490-2.
[38]	LUO W, HU H, CHANG R, et al. Pyruvate kinase M2 is a PHD3-stimulated coactivator for hypoxia-inducible factor 1[J]. Cell, 2011, 145(5): 732-744. DOI: 10.1016/j.cell.2011.03.054.
[39]	WONG N, OJO D, YAN J, et al. PKM2 contributes to cancer metabolism[J]. Cancer Lett, 2015, 356(2 Pt A): 184-191. DOI: 10.1016/j.canlet.2014.01.031.
[40]	FENG J, WU L, JI J, et al. PKM2 is the target of proanthocyanidin B2 during the inhibition of hepatocellular carcinoma[J]. J Exp Clin Cancer Res, 2019, 38(1): 204. DOI: 10.1186/s13046-019-1194-z.
[41]	LIU B, JIN J, ZHANG Z, et al. Shikonin exerts antitumor activity by causing mitochondrial dysfunction in hepatocellular carcinoma through PKM2-AMPK-PGC1α signaling pathway[J]. Biochem Cell Biol, 2019, 97(4): 397-405. DOI: 10.1139/bcb-2018-0310.
[42]	LING Y, YAN GJ, FENG F, et al. Association between cholesterol and liver regeneration and its significance and potential value in clinical treatment of liver failure[J]. J Clin Hepatol, 2022, 38(3): 708-713. DOI: 10.3969/j.issn.1001-5256.2022.03.044. 林镛, 颜耿杰, 冯逢, 等. 胆固醇与肝再生关系及其在肝衰竭治疗中的意义和潜在价值[J]. 临床肝胆病杂志, 2022, 38(3): 708-713. DOI: 10.3969/j.issn.1001-5256.2022.03.044.
[43]	WANG Y, LI X, CHEN Q, et al. Histone deacetylase 6 regulates the activation of M1 macrophages by the glycolytic pathway during acute liver failure[J]. J Inflamm Res, 2021, 14: 1473-1485. DOI: 10.2147/JIR.S302391.
[44]	WANG XF, SHI QL, WANG MG, et al. Experimental study on effect of Jiedu Huayu granules on hepatic mitochondrial permeability transition in rats with acute liver failure[J]. Liaoning J Tradit Chin Med, 2017, 44(10): 2186-2189. DOI: 10.13192/j.issn.1000-1719.2017.10.056. 王秀峰, 石清兰, 王明刚, 等. 解毒化瘀颗粒抑制急性肝衰竭大鼠肝线粒体通透性转换的实验研究[J]. 辽宁中医杂志, 2017, 44(10): 2186-2189. DOI: 10.13192/j.issn.1000-1719.2017.10.056.
[45]	ZHANG RZ, MAO DW, SUN KW, et al. Mechanism of action of Jieduhuayu granules for remission of oxidative stress in hepatocytes[J]. Chin J Hepatol, 2021, 29(12): 1188-1193. DOI: 10.3760/cma.j.cn501113-20210721-00349. 张荣臻, 毛德文, 孙克伟, 等. 解毒化瘀颗粒缓解肝细胞氧化应激的作用机制[J]. 中华肝脏病杂志, 2021, 29(12): 1188-1193. DOI: 10.3760/cma.j.cn501113-20210721-00349.

Relative Articles

[1]	Ru JIA, Pingping ZHANG, Yuan YUAN, Yiyang HU, Qin FENG. Differences and application value of plasma bile acids in tumors of the liver[J]. Journal of Clinical Hepatology, 2024, 40(10): 2042-2048. doi: 10.12449/JCH241018
[2]	ZHANG ZhongLin, YUAN YuFeng. Key operating points of laparoscopic hepatectomy for liver tumor in difficult locations[J]. Journal of Clinical Hepatology, 2020, 36(12): 2663-2666. doi: 10.3969/j.issn.1001-5256.2020.12.006
[3]	Li ShanShan, Zhang Ke, Cheng ShuJie, Yang JiHong, Gao Feng, Li JingHua. Current status and future perspectives of the application of medical 3D visualization technology in accurate surgery of liver tumors[J]. Journal of Clinical Hepatology, 2019, 35(5): 1114-1117. doi: 10.3969/j.issn.1001-5256.2019.05.042
[4]	Wang ZhiYu, Gu SanWei, Chen XiaoQian, Cai YanJun. Clonorchiasis misdiagnosed as hepatic tumor: a case report[J]. Journal of Clinical Hepatology, 2018, 34(3): 602-603. doi: 10.3969/j.issn.1001-5256.2018.03.033
[5]	Qi Fei, Tang YingMei. The mechanism of chenodeoxycholic acid and its derivatives in hepatobiliary tumor[J]. Journal of Clinical Hepatology, 2018, 34(5): 1115-1118. doi: 10.3969/j.issn.1001-5256.2018.05.041
[6]	Chen HaiOu, Liu Shi, Lin YiHe. Expression of M30 and CCL20 in serum in patients with HBV-related acute-on-chronic liver failure and their clinical significance[J]. Journal of Clinical Hepatology, 2018, 34(4): 806-809. doi: 10.3969/j.issn.1001-5256.2018.04.022
[7]	Lu NingNing, Sun Bin, Cui XiongWei, Long Jiang, Gao WenFeng, Zheng JiaSheng. Diagnosis and treatment of subcapsular hemorrhage after liver tumor ablation[J]. Journal of Clinical Hepatology, 2017, 33(12): 2326-2330. doi: 10.3969/j.issn.1001-5256.2017.12.014
[8]	Zhao Zhao, Qi WenQian, Zhao Ping. Research advances in insulin-like growth factor 1 receptor and its pathway in diagnosis and treatment of primary liver cancer[J]. Journal of Clinical Hepatology, 2017, 33(4): 763-768. doi: 10.3969/j.issn.1001-5256.2017.04.038
[9]	Kong Li, Jin Meng, Zhao SuXian. Role of tumor necrosis factor- alpha- induced protein 8-like 2 in development and progression of liver and gastrointestinal tumors[J]. Journal of Clinical Hepatology, 2017, 33(1): 175-179. doi: 10.3969/j.issn.1001-5256.2017.01.041
[10]	Chen Wei, Zhou Yun, Gong JianPing. Role of tumor-associated macrophages in development and progression of primary liver cancer[J]. Journal of Clinical Hepatology, 2016, 32(7): 1422-1424. doi: 10.3969/j.issn.1001-5256.2016.07.048
[11]	Wang JinWei, Zhang YaMin. Research advances in methods for determination of tumor boundary in hepatectomy[J]. Journal of Clinical Hepatology, 2016, 32(2): 374-377. doi: 10.3969/j.issn.1001-5256.2016.02.039
[12]	Lin Kun, Ci DanWangJiu, Chang ZhiHui, Liu ZhaoYu. Clinical value of circulating micro RNAs in hepatic,biliary and pancreatic carcinomas[J]. Journal of Clinical Hepatology, 2015, 31(5): 790-795. doi: 10.3969/j.issn.1001-5256.2015.05.040
[13]	Chen XuXiao, Chen YongJun. PI3K / Akt / mTOR signaling pathway and malignant hepatobiliary tumors[J]. Journal of Clinical Hepatology, 2015, 31(6): 989-991. doi: 10.3969/j.issn.1001-5256.2015.06.040
[14]	Wang WuChen, Zhou YongNing. Research progress in tumor- associated antigen antibodies for diagnosis of liver cancer[J]. Journal of Clinical Hepatology, 2014, 30(6): 573-576. doi: 10.3969/j.issn.1001-5256.2014.06.025
[15]	Fang ZiYan, Huang Long, Li Gong. Research progress in radiotherapy for liver tumors reported in 2013 ASTRO Annual Meeting[J]. Journal of Clinical Hepatology, 2014, 30(4): 383-385. doi: 10.3969/j.issn.1001-5256.2014.04.025
[16]	Ji Bo, Liu YaHui. Research advances in role of myeloid- derived suppressor cells in tumorigenesis[J]. Journal of Clinical Hepatology, 2014, 30(9): 939-943. doi: 10.3969/j.issn.1001-5256.2014.09.026
[17]	Chen MinHua. Standardization of thermal ablation in treatment of liver tumor[J]. Journal of Clinical Hepatology, 2013, 29(8): 561-563. doi: 10.3969/j.issn.1001-5256.2013.08.001
[19]	Yang BiWei, Gan YuHong, Ye ShengLong, Zhang BoHeng, Ren ZhengGang, Xia JingLin, Wang YanHong, Ge NingLing, Chen Yi, Li LiXin, Le Fan, Zhang Lan. Necrosis range and safety of radiofrequency combined with systemic chemotherapy and radiofrequency alone.[J]. Journal of Clinical Hepatology, 2004, 20(6): 364-365.

Supplements(0)

Cited By

Cited by

Periodical cited type(30)

1.	汪淑佳，俞黎. 多学科团队诊疗模式下的PDCA循环管理在梗阻性黄疸患者围术期护理中的应用效果分析. 中国社区医师. 2025(02): 96-98 .
2.	易衡，何芬，王曦，冯谦，唐杰，卿小琼，孙菲菲，陈重. 超声引导下PTCD治疗晚期MOJ疗效及预后因素分析. 武汉大学学报(医学版). 2024(07): 814-819 .
3.	李鸿. 老年晚期恶性梗阻性黄疸患者实时超声弹性成像定量分析对PTCD预后的预测价值. 昆明医科大学学报. 2023(01): 122-127 .
4.	李鸿. 老年晚期恶性梗阻性黄疸患者实时超声弹性成像定量分析对PTCD预后的评估价值. 昆明医科大学学报. 2023(02): 150-155 .
5.	梁亚丽，李馨，夏俊杰. 胰腺癌梗阻性黄疸患者经皮穿刺胆管引流术后发生胰腺炎的危险因素分析. 实用癌症杂志. 2023(08): 1321-1324 .
6.	杨立新，刘茜，周晶晶，唐亚丹，傅鹏，戴峰，白淑芬. 不同方法PTCD应用于梗阻性黄疸治疗中的体会. 现代医用影像学. 2023(12): 2229-2231+2235 .
7.	华建军. 超声引导下经皮肝穿刺胆管引流术治疗对阻塞性黄疸病人胆红素水平与肝功能的影响研究. 贵州医药. 2022(02): 226-227 .
8.	黄道琼，沈小叶，刘骏，刘月娥，陈瑜. 回授法在经皮肝穿刺胆管引流术后的应用. 介入放射学杂志. 2022(03): 294-297 .
9.	彭赵宏，张德志，施万印，赵本胜，熊壮，汪名权，宋文，陶龙香，刘斌，张帅，程翔. ~(125)I粒子支架治疗恶性梗阻性黄疸支架通畅时间的影响因素分析. 安徽医科大学学报. 2022(04): 645-649 .
10.	王玮，陈熙，罗丹，李启祥，尹合坤. 不同姑息性引流术对低位恶性梗阻性黄疸的近远期疗效及安全性分析. 当代医学. 2022(19): 39-42 .
11.	买买提·瓦司力，高旭升，司俊杰，徐峰. 经皮肝穿引流和支架植入在恶性梗阻性黄疸患者治疗的疗效评价. 新疆医学. 2022(07): 770-772+809 .
12.	王颖. 彩超引导经皮穿刺肝胆管引流术治疗梗阻性黄疸的临床研究. 中国医疗器械信息. 2022(15): 123-125 .
13.	宋飞，向盈盈，车佳音，李红阳，徐文勇，魏凌潇，黄明. 胆道~(125)I粒子支架与金属裸支架治疗Bismuth Corlette Ⅲ型胆管癌合并梗阻性黄疸的临床对比. 昆明医科大学学报. 2022(11): 85-89 .
14.	冉庆. ERCP联合PTCD胆总管支架置入胆管引流治疗恶性梗阻性黄疸的临床价值. 医学食疗与健康. 2021(04): 86-87 .
15.	王锦程，余佩和，苏松，李波. 经内镜鼻胆管引流术与经内镜胆道支架置入术在低位恶性梗阻性黄疸术前胆道引流效果比较的Meta分析. 临床肝胆病杂志. 2021(04): 863-867 . 本站查看
16.	马博，周军，周京涛，李建刚，王俊. 胆道支架植入治疗恶性梗阻性黄疸术后并发症的发生因素分析. 现代生物医学进展. 2021(07): 1283-1286 .
17.	张建松，侯森，崔虎啸. 超声引导下经皮肝穿刺胆道引流联合胆管复合支架置入术治疗晚期肝外胆管癌的效果. 癌症进展. 2021(09): 931-934 .
18.	张华安，周晓芳，蒋易君，张淏嘉. NRS-2002联合炎症反应标志物预测恶性梗阻性黄疸患者预后的Nomogram模型构建. 山东医药. 2021(16): 35-40 .
19.	石书伟，王劲. 经皮肝穿刺胆道引流联合金属支架植入术对恶性梗阻性黄疸的影响. 黑龙江医学. 2021(15): 1608-1609 .
20.	宋英茜，陶冶. 梗阻性黄疸经皮肝穿刺胆道引流术后胆道感染的病原菌特点及其危险因素分析. 中国实用乡村医生杂志. 2021(02): 33-36 .
21.	张志强，韩涛，崔钢，王奕，蔡恒烈，廖骞. 右肝管入路单通道横跨左右肝管引流治疗汇管区恶性梗阻性黄疸的临床研究. 中国普通外科杂志. 2021(12): 1503-1508 .
22.	傅建英. 内镜介入治疗急性梗阻性黄疸的疗效及对患者炎症因子的影响. 中外医疗. 2021(33): 57-60 .
23.	李蔚，王锡斌，崔卫东，杨青，刘会苗，杨金雨，王锡斌. 超声引导下经皮经肝胆管穿刺引流术治疗急性梗阻性化脓性胆管炎患者疗效分析. 实用肝脏病杂志. 2020(03): 447-450 .
24.	李磊. 胆道支架联合经皮肝穿刺胆管引流术对晚期恶性梗阻性黄疸的临床应用价值. 名医. 2020(08): 85-86 .
25.	张蓓，答秀维，张乐. 经皮肝穿刺胆道外引流治疗恶性梗阻性黄疸疗效及对患者细胞免疫功能、血清直接胆红素、超敏C反应蛋白水平的影响. 陕西医学杂志. 2020(10): 1249-1252 .
26.	朱超，刘会春，胡小四，庞青，陈邦邦，李传涛. 胆道双支架联合~(125)I粒子腔内照射治疗恶性肝门部胆道梗阻的疗效分析. 介入放射学杂志. 2020(11): 1100-1104 .
27.	姜磊，都晓英，孙医学，张大坤，周凯，徐建中，陈芳芳. PTBS术治疗恶性梗阻性黄疸的临床价值及预后因素分析. 蚌埠医学院学报. 2019(09): 1202-1205+1209 .
28.	江新华. 64层螺旋CT3D成像与MRCP成像技术对胆道梗阻性疾病的诊断价值. 江西医药. 2019(11): 1336-1340 .
29.	吴子鑫，吴申伟. 经皮肝穿刺胆道支架植入治疗对恶性梗阻性黄疸患者肝功能指标、炎症指标的影响. 齐齐哈尔医学院学报. 2019(24): 3098-3099 .
30.	武飞. 经皮肝穿刺胆管引流术与Roux-en-Y胆肠吻合术治疗恶性梗阻性黄疸患者的对比研究. 中国药物与临床. 2019(23): 4098-4100 .

Other cited types(4)

Proportional views

Proportional views

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

Figures(1)

Get Citation

PDF

XML

Article Metrics

Article views (1755) PDF downloads(170)

Association between glycolysis and mitochondrial dysfunction and its potential value in liver diseases

DOI: 10.3969/j.issn.1001-5256.2022.08.042