中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 35 Issue 6
Jun.  2019
Turn off MathJax
Article Contents

The role of the NOD-like receptor family, pyrin domain-containing protein 3 inflammasome in nonalcoholic steatohepatitis

DOI: 10.3969/j.issn.1001-5256.2019.06.045
Research funding:

 

  • Received Date: 2018-12-24
  • Published Date: 2019-06-20
  • Nonalcoholic steatohepatitis (NASH) is an important pathological stage of nonalcoholic fatty liver disease characterized by hepatocyte fatty degeneration, liver injury, and liver inflammation and can further develop into liver cirrhosis and hepatocellular carcinoma. The NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome is a multi-protein complex in cells and can induce cell apoptosis and expand inflammatory response by activating caspase-1 and releasing mature inflammatory factors such as interleukin-1β and interleukin-18. Recent studies have found that NLRP3 inflammasome may participate in the development and progression of NASH. Therefore, this article summarizes the role of NLRP3 inflammasome in NASH, so as to provide a theoretical basis for future research and treatment.

     

  • loading
  • [1]National Workshop on Fatty Liver and Alcoholic Liver Disease, Chinese Society of Hepatology, Chinese Medical Association;Fatty Liver Expert Committee, Chinese Medical Doctor Association.Guidelines of prevention and treatment for nonalcoholic fatty liver disease:A 2018 update[J].J Clin Hepatol, 2018, 34 (5) :947-957. (in Chinese) 中华医学会肝病学分会脂肪肝和酒精性肝病学组, 中国医师协会脂肪性肝病专家委员会.非酒精性脂肪性肝病防治指南 (2018年更新版) [J].临床肝胆病杂志, 2018, 34 (5) :947-957.
    [2]WU L, ZHANG J, MA WT, et al.Xiayuxue decoction inhibits methionine-choline-deficient-induced nonalcoholic steatohepatitis in mice[J/CD].Chin J Liver Dis:Electronic Version, 2018, 10 (3) :48-55. (in Chinese) 吴柳, 张洁, 马文婷, 等.下瘀血汤对胆碱蛋氨酸缺乏诱导的小鼠非酒精性脂肪性肝炎的抑制作用[J/CD].中国肝脏病杂志:电子版, 2018, 10 (3) :48-55.
    [3]LI ZZ, XUE J, CHEN P, et al.Prevalence of nonalcoholic fatty liver disease in mainland of China:A meta-analysis of published studies[J].J Gastroen Hepatol, 2014, 29 (1) :42-51.
    [4]ZENG MD.Achievements and perspectives in nonalcoholic fatty liver diseases[J].J Prac Hepatol, 2016, 19 (2) :129-131. (in Chinese) 曾民德.非酒精性脂肪性肝病:回顾历史, 展望未来[J].实用肝脏病杂志, 2016, 19 (2) :129-131.
    [5]HARA H, TSUCHIYA K, KAWAMURA I, et al.Phosphorylation of the adaptor ASC acts as a molecular switch that controls the formation of speck-like aggregates and inflammasome activity[J].Nat Immunol, 2013, 14 (12) :1247.
    [6]SZABO G, PETRASEK J.Inflammasome activation and function in liver disease[J].Nat Rev Gastro Hepat, 2015, 12 (7) :387.
    [7]LISTON A, MASTERS SL.Homeostasis-altering molecular processes as mechanisms of inflammasome activation[J].Nat Rev Immunol, 2017, 17 (3) :208-214.
    [8]DOSTERT C, PETRILLI V, BRUGGEN RV, et al.Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica[J].Science, 2008, 320 (5876) :674-677.
    [9]JO EK, KIM JK, SHIN DM, et al.Molecular mechanisms regulating NLRP3 inflamma-some activation[J].Cell Mol Immunol, 2016, 13 (2) :148-159.
    [10]RAJAMAKI K, LAPPALAINEN J, OORNI K, et al.Cholesterol crystals activate the NLRP3 inflammasome in human macrophages:A novel link between cholesterol metabolism and inflammation[J].PLo S One, 2010, 5 (7) :e11765.
    [11]LAMKANFI M, DIXIT VM.Inflammasomes and their roles in health and disease[J].Annu Rev Cell Dev Biol, 2012, 28 (28) :137.
    [12]IYER SS, HE Q, JANCZY JR, et al.Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation[J].Immunity, 2013, 39 (2) :311-323.
    [13]DUEWELL P, KONO H, RAYNER KJ, et al.NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J].Nature, 2010, 464 (7293) :1357-1361.
    [14]SANMAN LE, QIAN Y, EISELE NA, et al.Disruption of glycolytic flux is a signal for inflammasome signaling and pyroptotic cell death[J].Elife, 2016, 5:e13663.
    [15]SONG N, LIU ZS, XUE W, et al.NLRP3 phosphorylation is an essential priming event for inflammasome activation[J].Mol Cell, 2017, 68:185-197.e6.
    [16]ZHANG ZR, MESZARIS G, HE WT, et al.Protein kinase D at the Golgi controls NLRP3 inflammasome activation[J].J Exp Med, 2017, 214 (9) :2671-2693.
    [17]BEDNASH JS, MALLAMPALLI RK.Regulation of inflammasomes by ubiquitination[J].Cell Mol Immunol, 2016, 13 (6) :722-728.
    [18]ZHONG Z, UMEMURA A, SANCHEZ-LOPEZ E, et al.NF-κB restricts inflammasome activation via elimination of damaged mitochondria[J].Cell, 2016, 164 (5) :896-910.
    [19]GUARDA G, BRAUN M, STAEHLI F, et al.Type I interferon inhibits interleukin-1 production and inflammasome activation[J].Immunity, 2011, 34 (2) :213-223.
    [20]MISHRA BB, RATHINAM VA, MARTENS GW, et al.Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β[J].Nat Immunol, 2013, 14 (1) :52-60.
    [21]BAUERNFEIND F, RIEGER A, SCHILDBERG FA, et al.NL-RP3 inflammasome activity is negatively controlled by miR-223[J].J Immunol, 2012, 189 (8) :4175-4181.
    [22]WREE A, EGUCHI A, MCGEOUGH MD, et al.NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice[J].Hepatology, 2014, 59 (3) :898-910.
    [23]CSAK T, PILLAI A, GANZ M, et al.Both bone marrow-derived and non-bone marrow-derived cells contribute to AIM2and NLRP3 inflammasome activation in a MyD88-dependent manner in dietary steatohepatitis[J].Liver Int, 2014, 34 (9) :1402-1413.
    [24]LIU X, ZHANG Z, RUAN J, et al.Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores[J].Nature, 2016, 535 (7610) :153-158.
    [25]CSAK T, GANZ M, PESPISA J, et al.Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells[J].Hepatology, 2011, 54 (1) :133-144.
    [26]WREE A, MCGEOUGH MD, PENA CA, et al.NLRP3 inflammasome activation is required for fibrosis development in NAFLD[J].J Mol Med, 2014, 92 (10) :1069-1082.
    [27]XU B, JIANG M, CHU Y, et al.Gasdermin D plays a key role as a pyroptosis executor of non-alcoholic steatohepatitis in humans and mice[J].J Hepatol, 2018, 68 (4) :773-782.
    [28]QIU TM, PEI P, YAO XF, et al.Taurine attenuates arsenicinduced pyroptosis and nonalcoholic steatohepatitis by inhibiting the autophagic-inflammasomal pathway[J].Cell Death Dis, 2018, 9 (10) :946.
    [29]MRIDHA AR, WREE A, ROBERTSON AAB, et al.NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice[J].J Hepatol, 2017, 66 (5) :1037-1046.
    [30]LYONS CL, KENNEDY EB, ROCHE HM.Metabolic inflammation-differential modulation by dietary constituents[J].Nutrients, 2016, 8 (5) :e247.
    [31]FINUCANE OM, LYONS CL, MURPHY AM, et al.Monounsaturated fatty acid-enriched high-fat diets impede adipose NLRP3 inflammasome-mediated IL-1βsecretion and insulin resistance despite obesity[J].Diabetes, 2015, 64 (6) :2116-2128.
    [32]FERNANDES-ALNEMRI T, KANG S, ANDERSON C, et al.Cutting edge:TLR signaling licenses IRAK1 for rapid activation of the NLRP3 inflammasome[J].J Immunol, 2013, 191 (8) :3995-3999.
    [33]IOANNOU GN, HAIGH WG, THORNING D, et al.Hepatic cholesterol crystals and crown-like structures distinguish NASH from simple steatosis[J].J Lipid Res, 2013, 54 (5) :1326.
    [34]IOANNOU GN, van ROOYEN DM, SAVARD C, et al.Cholesterol-lowering drugs cause dissolution of cholesterol crystals and disperse Kupffer cell crown-like structures during resolution of NASH[J].J Lipid Res, 2015, 56 (2) :277-285.
    [35]COLLR C, ROBERTSON AAB, CHAE JJ, et al.A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases[J].Nat Med, 2015, 21 (3) :248-255.
    [36]BARREYRO FJ, SILVIA H, PAOLA VF, et al.The pan-caspase inhibitor Emricasan (IDN-6556) decreases liver injury and fibrosis in a murine model of non-alcoholic steatohepatitis[J].Liver Int, 2015, 35 (3) :953-966.
    [37]DIXON LJ, FLASK CA, PAPOUCHADO BG, et al.Caspase-1 as a central regulator of high fat diet-induced non-alcoholic steatohepatitis[J].PLo S One, 2013, 8:e56100.
    [38]WANG HG, SUN WL, ZHONG PY, et al.Effect of exogenous hydrogen sulfide on expression of NLRP3 inflammasome in hepatocytes[J].Chin J Pathophysiol, 2018, 34 (1) :118-122. (in Chinese) 王红钢, 孙伟力, 钟培育, 等.外源性硫化氢对肝细胞NLRP3炎症小体的影响[J].中国病理生理杂志, 2018, 34 (1) :118-122.
    [39]WU MB, ZHANG WF, GONG JP, et al.Wortmannin inhibits the activity of NLRP3 in Kupffer cells through the Chemerin/CMKLR pathway and relieves nonalcoholic fatty liver in mice[J].Chongqing Med, 2018, 47 (17) :2279-2284. (in Chinese) 吴明兵, 张文锋, 龚建平, 等.渥曼青霉素通过Chemerin/CMKLR1途径抑制Kupffer细胞NLRP3的活性缓解小鼠非酒精性脂肪肝[J].重庆医学, 2018, 47 (17) :2279-2284.
    [40]TANG Y, CAO G, MIN X, et al.Cathepsin B inhibition ameliorates the non-alcoholic steatohepatitis through suppressing Caspase-1 activation[J].J Physiol Biochem, 2018, 74 (4) :503-510.
    [41]KIM SH, KIM G, HAN DH, et al.Ezetimibe ameliorates steatohepatitis via AMP activated protein kinase-TFEB-mediated activation of autophagy and NLRP3 inflammasome inhibition[J].Autophagy, 2017, 13 (10) :1767-1781.
    [42]XIAO J, WANG F, LIONG EC, et al.Lycium barbarum polysaccharides improve hepatic injury through NFkappa-B and NLRP3/6 pathways in a methionine choline deficient diet steatohepatitis mouse model[J].Int J Biol Macromol, 2018, 120 (Pt B) :1480-1489.
    [43]CABRERA D, WERR A, POVERO D, et al.Andrographolide ameliorates inflammation and fibrogenesis and attenuates inflammasome activation in experimental non-alcoholic steatohepatitis[J].Sci Rep, 2017, 7 (1) :3491.
    [44]CHEN Y, HE XX, YUAN XX, et al.NLRP3 Inflammasome formation and activation in nonalcoholic steatohepatitis:Therapeutic target for antimetabolic syndrome remedy FTZ[J].Oxid Med Cell Longev, 2018, 2018:2901871.
  • 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

    Article Metrics

    Article views (1347) PDF downloads(238) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return