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Volume 42 Issue 1
Jan.  2019
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Xiumei WANG, Changping LI. Molecular mechanism of MicroRNA-21 in non-alcoholic fatty liver disease[J]. Journal of Molecular Imaging, 2019, 42(1): 87-90. doi: 10.12122/j.issn.1674-4500.2019.01.20
Citation: Xiumei WANG, Changping LI. Molecular mechanism of MicroRNA-21 in non-alcoholic fatty liver disease[J]. Journal of Molecular Imaging, 2019, 42(1): 87-90. doi: 10.12122/j.issn.1674-4500.2019.01.20

Molecular mechanism of MicroRNA-21 in non-alcoholic fatty liver disease

doi: 10.12122/j.issn.1674-4500.2019.01.20
  • Received Date: 2018-04-03
  • Publish Date: 2019-01-01
  • MicroRNAs (miRNAs) are endogenous, non-coding small RNAs of approximately 19-25 nucleotides in length, which have a variety of regulatory roles in cells.Such as regulating the proliferation, apoptosis and differentiation of different cells.etc, mainly by targeting completely or incompletely the 3′-UTR region of mRNAs affects the translation and post-transcriptional regulation of targeted gene expression. Recent studies have found that microRNA-21 was involved in the pathogenesis of non-alcoholic fatty liver disease, which is related to its progression and prognosis. Comprehensive research found that the expression of microRNA-21 can be involved in the development of non-alcoholic fatty liver disease and its related complications through multiple targets, such as HMGCR, LRP6, PPAR-α. This article reviews the role and molecular mechanism of microRNA-21 in different stages of development of non-alcoholic fatty liver disease, and provides a basis for further research on the treatment of non-alcoholic fatty liver disease.

     

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  • [1]
    Hardy T, Oakley F, Anstee QM, et al. Nonalcoholic fatty liver disease: pathogenesis and disease spectrum[J]. Annu Rev Pathol, 2016, 11(11): 451-96
    [2]
    He Z, Hu C, Jia WP. miRNAs in non-alcoholic fatty liver disease[J]. Front Med, 2016, 10(4): 389-96 doi: 10.1007/s11684-016-0468-5
    [3]
    Jhaas Jt, Francque S. Pathophysiology and mechanisms of nonalcoholic fatty liver disease[J]. Annu Rev physiol, 2016, 78(2): 181-205
    [4]
    Shubham K, Vinay L, Vinod PK. Systems-level organization of non-alcoholic fatty liver disease progression network[J]. Mol Biosyst, 2017, 13(9): 1898-911 doi: 10.1039/C7MB00013H
    [5]
    Janssen AW, Houben T, Katiraei S, et al. Modulation of the gut microbiota impacts nonalcoholic fatty liver disease: a potential role for bile acids[J]. J Lipid Res, 2017, 58(7): 1399-416 doi: 10.1194/jlr.M075713
    [6]
    Bhanji RA, Narayanan P, Allen AM, et al. Sarcopenia in hiding: The risk and consequence of underestimating muscle dysfunction in NASH[J]. Hepatology, 2017, 66(5): 512-9
    [7]
    Meex RR. Watt matthew J. hepatokines: linking nonalcoholic fatty liver disease and insulin resistance[J]. Nat Rev Endocrinol, 2017, 13(9): 509-20 doi: 10.1038/nrendo.2017.56
    [8]
    Mehta R, Otgonsuren M, Younoszai Z, et al. Circulating miRNA in patients with non-alcoholic fatty liver disease and coronary artery disease[J]. BMJ Open Gastroenterol, 2016, 3(1): e000096-102 doi: 10.1136/bmjgast-2016-000096
    [9]
    Singh AK, Aryal B, Zhang X, et al. Posttranscriptional regulation of lipid metabolism by non-coding RNAs and RNA binding proteins[J]. Semin Cell Dev Biol, 2017, 11(2): 026-35
    [10]
    Tryndyak VP, Marrone AK, Latendresse JR, et al. MicroRNA changes, activation of progenitor cells and severity of liver injury in mice induced by choline and folate deficiency[J]. J Nutr Biochem, 2016, 28(1): 83-90
    [11]
    Becker PP, Rau M, Schmitt J, et al. Performance of serum microRNAs-122, -192 and-21 as biomarkers in patients with Non-Alcoholic steatohepatitis[J]. PLoS One, 2015, 10(11): e0142661-72 doi: 10.1371/journal.pone.0142661
    [12]
    Huang Y, He Y, Li J. MicroRNA-21: a central regulator of fibrotic diseases via various targets[J]. Curr Pharm Des, 2015, 21(17): 2236-42 doi: 10.2174/1381612820666141226095701
    [13]
    Vinciguerra M, Sgroi A, Veyrat-Durebex C, et al. Unsaturated fatty acids inhibit the expression of tumor suppressor phosphatase and tensin homolog (PTEN) via microRNA-21 up-regulation in hepatocytes[J]. Hepatology, 2009, 49(4): 1176-84 doi: 10.1002/hep.22737
    [14]
    Ahn J, Lee H, Jung CH, et al. Lycopene inhibits hepatic steatosis via microRNA-21-induced downregulation of fatty acid-binding protein 7 in mice fed a high-fat diet[J]. Mol Nutr Food Res, 2012, 56(11): 1665-74 doi: 10.1002/mnfr.v56.11
    [15]
    Sun CZ, Huang FZ, Liu XY, et al. miR-21 regulates triglyceride and cholesterol metabolism in non-alcoholic fatty liver disease by targeting HMGCR[J]. Int J Mol Med, 2015, 35(3): 847-53 doi: 10.3892/ijmm.2015.2076
    [16]
    Zhao XY. Roles of MicroRNA-21 in the Pathogenesis of Insulin Resistance and Diabetic Mellitus-induced Non-alcoholic Fatty Liver Disease[J]. Acta Academiae Medicinae Sinicae, 2016, 38(2): 144-9
    [17]
    Li CP, Li HJ, Nie J, et al. Mutation of miR-21 targets endogenous lipoprotein receptor-related protein 6 and nonalcoholic fatty liver disease[J]. Am J Transl Res, 2017, 9(2): 715-21
    [18]
    Go GW. Low-Density lipoprotein Receptor-Related protein 6 (LRP6) is a novel nutritional therapeutic target for hyperlipidemia, Non-Alcoholic fatty liver disease, and atherosclerosis[J]. Nutrients, 2015, 7(6): 4453-64 doi: 10.3390/nu7064453
    [19]
    Go GW, Srivastava R, Hernandez-Ono AA, et al. The combined hyperlipidemia caused by impaired Wnt-LRP6 signaling is reversed by Wnt3a rescue[J]. Cell Metab, 2014, 19(2): 209-20 doi: 10.1016/j.cmet.2013.11.023
    [20]
    Francque S, Verrijken A, Caron S, et al. PPAR alpha gene expression correlates with severity and histological treatment response in patients with non-alcoholic steatohepatitis[J]. J Hepatol, 2015, 63(1): 164-73 doi: 10.1016/j.jhep.2015.02.019
    [21]
    Ren TT, Zhu JJ, Zhu LL, et al. The combination of blueberry juice and probiotics ameliorate Non-Alcoholic steatohepatitis (NASH) by affecting SREBP-1c/PNPLA-3 pathway via PPAR-alpha[J]. Nutrients, 2017, 9(3): 258-63 doi: 10.3390/nu9030258
    [22]
    Loyer X, Paradis V, Henique C, et al. Liver microRNA-21 is overexpressed in non-alcoholic steatohepatitis and contributes to the disease in experimental models by inhibiting PPAR alpha expression[J]. Gut, 2016, 65(11): 1882-94 doi: 10.1136/gutjnl-2014-308883
    [23]
    Rodrigues PM, Afonso MB, Simao AL, et al. miR-21 ablation and obeticholic acid ameliorate nonalcoholic steatohepatitis in mice[J]. Cell Death Dis, 2017, 8(5): e2825-32 doi: 10.1038/cddis.2017.246
    [24]
    Dattaroy D, Pourhoseini S, Das S, et al. Micro-RNA 21 inhibition of SMAD7 enhances fibrogenesis via leptin-mediated NADPH oxidase in experimental and human nonalcoholic steatohepatitis[J]. Am J Physiol Gastrointest Liver Physiol, 2015, 308(4): G298-312 doi: 10.1152/ajpgi.00346.2014
    [25]
    Yang F, Luo L, Zhu ZD, et al. Chlorogenic acid inhibits liver fibrosis by blocking the miR-21-Regulated TGF-β1/Smad7 signaling pathwayand[J]. Frontiers Pharmacol, 2017, 8(9): 929-36
    [26]
    Jin K, Li T, Sanchez-Duffhues G, et al. Involvement of inflammation and its related microRNAs in hepatocellular carcinoma[J]. Oncotarget, 2017, 8(13): 22145-65
    [27]
    Wu KM, Ye CH, Lin L, et al. Inhibiting miR-21 attenuates experimental hepatic fibrosis by suppressing both the ERK1 pathway in HSC and hepatocyte EMT[J]. Clin Sci, 2016, 130(16): 1469-80 doi: 10.1042/CS20160334
    [28]
    Ning ZW, Luo XY, Wang GZ, et al. MicroRNA-21 mediates angiotensin II-Induced liver fibrosis by activating NLRP3 inflammasome/IL-1 beta axis via targeting Smad7 and spry1[J]. Antioxid Redox Signal, 2017, 27(1): 1-20 doi: 10.1089/ars.2016.6669
    [29]
    Caviglia JM, Yan J, Jang MK, et al. MicroRNA-21 and dicer are dispensable for hepatic stellate cell activation and the development of liver fibrosis[J]. Hepatology, 2018, 67(6): 2414-29 doi: 10.1002/hep.29627
    [30]
    Jiang JH, Yang PP, Guo Z, et al. Overexpression of microRNA-21 strengthens stem cell-like characteristics in a hepatocellular carcinoma cell line[J]. World J Surg Oncol, 2016, 14(1): 10-9
    [31]
    Wang ZP, Yang H, Ren L. MiR-21 promoted proliferation and migration in hepatocellular carcinoma through negative regulation of Navigator-3[J]. Biochem Biophys Res Commun, 2015, 464(4): 1228-34 doi: 10.1016/j.bbrc.2015.07.110
    [32]
    Mao B, Xiao H, Zhang Z, et al. MicroRNA21 regulates the expression of BTG2 in HepG2 liver cancer cells[J]. Molecular medicine reports, 2015, 12(4): 4917-24 doi: 10.3892/mmr.2015.4051
    [33]
    Hu SX, Tao RY, Wang SY, et al. MicroRNA-21 promotes cell proliferation in human hepatocellular carcinoma partly by targeting HEPN1[J]. Tumour Biol, 2015, 36(7): 5467-72 doi: 10.1007/s13277-015-3213-9
    [34]
    Wagenaar TR, Zabludoff S, Ahn S, et al. Anti-miR-21 suppresses hepatocellular carcinoma growth via broad transcriptional network deregulation[J]. Mol Cancer Res, 2015, 13(6): 1009-21 doi: 10.1158/1541-7786.MCR-14-0703
    [35]
    Wu H, Ng R, Chen X, et al. MicroRNA-21 is a potential Link between non-alcoholic fatty liver disease and hepatocellular carcinoma via modulation of the HBP1-p53-Srebp1c pathway[J]. Gut, 2015, 65(11): 1850-60
    [36]
    He W, Wang C, Mu R, et al. MiR-21 is required for anti-tumor immune response in mice: an implication for its bi-directional roles[J]. Oncogene, 2017, 36(29): 4212-23 doi: 10.1038/onc.2017.62
    [37]
    Lai SC, Iwakiri Y. Is miR-21 a potent target for liver fibrosis[J]. Hepatology, 2018, 67(6): 2082-4 doi: 10.1002/hep.29774
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