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炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制

张文杰 孙迪阳 王培

张文杰, 孙迪阳, 王培. 炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制[J]. 药学实践与服务, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
引用本文: 张文杰, 孙迪阳, 王培. 炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制[J]. 药学实践与服务, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
ZHANG Wenjie, SUN Diyang, WANG Pei. The role and mechanism of inflammasome-associated pyroptosis in nonalcoholic fatty liver disease[J]. Journal of Pharmaceutical Practice and Service, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
Citation: ZHANG Wenjie, SUN Diyang, WANG Pei. The role and mechanism of inflammasome-associated pyroptosis in nonalcoholic fatty liver disease[J]. Journal of Pharmaceutical Practice and Service, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051

炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制

doi: 10.3969/j.issn.1006-0111.201902051

The role and mechanism of inflammasome-associated pyroptosis in nonalcoholic fatty liver disease

  • 摘要: 非酒精性脂肪肝病包含单纯性脂肪肝、非酒精性脂肪肝炎和肝硬化等一系列病变,是造成肝硬化、肝细胞癌症的主要因素和肝脏器官移植的重要诱因。非酒精性脂肪肝的发病机制尚不明确,除了加强运动、改善饮食习惯外,目前尚无公认有效的药物治疗方式。细胞焦亡是一种新发现的程序性细胞死亡方式,依赖于天冬氨酸特异性半胱氨酸蛋白酶1(caspase-1)或caspase-11等介导的炎性小体的激活。细胞焦亡过程中常伴有炎症反应的发生,而炎症小体则是细胞产生焦亡和炎症反应所必需的多聚体蛋白复合物,其主要功能是活化caspase-1,从而间接调控炎症因子白介素1(IL-1)和IL-18的表达和分泌。最近的研究表明,细胞焦亡和炎症小体在非酒精性脂肪肝病的发生发展中起重要作用。针对该领域的最新研究进行综述,以期为非酒精性脂肪肝的防治提供新的科学认识和信息。
  • [1] VILLANUEVA M T. Conscious uncoupling in NASH[J]. Nat Rev Drug Discov,2017,16(4):239
    [2] NEUSCHWANDER-TETRI B A. Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites[J]. Hepatology,2010,52(2):774-788
    [3] MARRA F, SVEGLIATI-BARONI G. Lipotoxicity and the gut-liver axis in NASH pathogenesis[J]. J Hepatol,2018,68(2):280-295
    [4] PEVERILL W, POWELL L, SKOIEN R. Evolving concepts in the pathogenesis of NASH: beyond steatosis and inflammation[J]. Int J Mol Sci,2014,15(5):8591-8638
    [5] LAZIC M, INZAUGARAT M E, POVERO D, et al. Reduced dietary omega-6 to omega-3 fatty acid ratio and 12/15-lipoxygenase deficiency are protective against chronic high fat diet-induced steatohepatitis[J]. Plos One,2014,9(9):e107658
    [6] ABDELMALEK M F, SUZUKI A, GUY C, et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease[J]. Hepatology,2010,51(6):1961-1971
    [7] IOANNOU G N, VAN ROOYEN D M, 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
    [8] MIELE L C, MARRONE G, LAURITANO C, et al. Gut-liver axis and microbiota in NAFLD: insight pathophysiology for novel therapeutic target[J]. Curr Pharm Des,2013,19(29):5314-5324
    [9] SCHRODER K, TSCHOPP J. The inflammasomes[J]. Cell,2010,140(6):821-832
    [10] MINKIEWICZ J, DE RIVERO VACCARI J P, KEANE R W. Human astrocytes express a novel NLRP2 inflammasome[J]. Glia,2013,61(7):1113-1121
    [11] Wlodarska M, Thaiss CA, Nowarski R, et al. NLRP6 inflammasome orchestrates the colonic host-microbial interface by regulating goblet cell mucus secretion[J]. Cell,2014,156(5):1045-1059
    [12] OHASHI K, WANG Z J, YANG Y M, et al. NOD-like receptor C4 inflammasome regulates the growth of colon cancer liver metastasis in NAFLD[J]. Hepatology,2019:30693
    [13] DING J J, WANG K, LIU W, et al. Pore-forming activity and structural autoinhibition of the gasdermin family[J]. Nature,2016,535(7610):111-116
    [14] WREE A, MCGEOUGH M D, PEÑA C A, et al. NLRP3 inflammasome activation is required for fibrosis development in NAFLD[J]. J Mol Med,2014,92(10):1069-1082
    [15] MATSUZAKA T, ATSUMI A, MATSUMORI R, et al. Elovl6 promotes nonalcoholic steatohepatitis[J]. Hepatology,2012,56(6):2199-2208
    [16] WEN H T, GRIS D, LEI Y, et al. Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling[J]. Nat Immunol,2011,12(5):408-415
    [17] WREE A, EGUCHI A, MCGEOUGH M D, et al. NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice[J]. Hepatology,2014,59(3):898-910
    [18] MRIDHA A R, WREE A, ROBERTSON A A B, et al. NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice[J]. J Hepatol,2017,66(5):1037-1046
    [19] YANG S J, LIM Y. Resveratrol ameliorates hepatic metaflammation and inhibits NLRP3 inflammasome activation[J]. Metabolism,2014,63(5):693-701
    [20] 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
    [21] MIURA K, KODAMA Y, INOKUCHI S, et al. Toll-like receptor 9 promotes steatohepatitis by induction of interleukin-1β in mice[J]. Gastroenterology,2010,139(1):323-334.e7
    [22] STIENSTRA R, SAUDALE F, DUVAL C, et al. Kupffer cells promote hepatic steatosis via interleukin-1β-dependent suppression of peroxisome proliferator-activated receptor α activity[J]. Hepatology,2010,51(2):511-522
    [23] VANDANMAGSAR B, YOUM Y, RAVUSSIN A, et al. The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance[J]. Nat Med,2011,17(2):179-188
    [24] PETRASEK J, BALA S S, CSAK T, et al. IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice[J]. J Clin Invest,2012,122(10):3476-3489
    [25] WITEK R P, STONE W C, KARACA F G, et al. Pan-caspase inhibitor VX-166 reduces fibrosis in an animal model of nonalcoholic steatohepatitis[J]. Hepatology,2009,50(5):1421-1430
    [26] KIM S H, KIM G, HAN D H, 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
    [27] HENAO-MEJIA J, ELINAV E, JIN C C, et al. Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity[J]. Nature,2012,482(7384):179-185
    [28] DE MINICIS S, RYCHLICKI C, AGOSTINELLI L, et al. Dysbiosis contributes to fibrogenesis in the course of chronic liver injury in mice[J]. Hepatology,2014,59(5):1738-1749
    [29] CSAK T, PILLAI A, GANZ M, et al. Both bone marrow-derived and non-bone marrow-derived cells contribute to AIM2 and NLRP3 inflammasome activation in a MyD88-dependent manner in dietary steatohepatitis[J]. Liver Int,2014,34(9):1402-1413
    [30] MURPHY A J, KRAAKMAN M J, KAMMOUN H L, et al. IL-18 production from the NLRP1 inflammasome prevents obesity and metabolic syndrome[J]. Cell Metab,2016,23(1):155-164
    [31] ANITHA M, REICHARDT F, TABATABAVAKILI S, et al. Intestinal dysbiosis contributes to the delayed gastrointestinal transit in high-fat diet fed mice[J]. Cell Mol Gastroenterol Hepatol,2016,2(3):328-339
    [32] CHEN G Y, LIU M C, WANG F Y, et al. A functional role for Nlrp6 in intestinal inflammation and tumorigenesis[J]. J Immunol,2011,186(12):7187-7194
    [33] ZHANG Q, RAOOF M, CHEN Y, et al. Circulating mitochondrial DAMPs cause inflammatory responses to injury[J]. Nature,2010,464(7285):104-107
    [34] SUN Q, LOUGHRAN P, SHAPIRO R, et al. Redox-dependent regulation of hepatocyte absent in melanoma 2 inflammasome activation in sterile liver injury in mice[J]. Hepatology,2017,65(1):253-268
    [35] WATANABE A, SOHAIL M A, GOMES D A, et al. Inflammasome-mediated regulation of hepatic stellate cells[J]. Am J Physiol Gastrointest Liver Physiol,2009,296(6):G1248-G1257
    [36] WREE A, MCGEOUGH M D, INZAUGARAT M E, et al. NLRP3 inflammasome driven liver injury and fibrosis: Roles of IL-17 and TNF in mice[J]. Hepatology,2018,67(2):736-749
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  • 收稿日期:  2019-02-22
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炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制

doi: 10.3969/j.issn.1006-0111.201902051

摘要: 非酒精性脂肪肝病包含单纯性脂肪肝、非酒精性脂肪肝炎和肝硬化等一系列病变,是造成肝硬化、肝细胞癌症的主要因素和肝脏器官移植的重要诱因。非酒精性脂肪肝的发病机制尚不明确,除了加强运动、改善饮食习惯外,目前尚无公认有效的药物治疗方式。细胞焦亡是一种新发现的程序性细胞死亡方式,依赖于天冬氨酸特异性半胱氨酸蛋白酶1(caspase-1)或caspase-11等介导的炎性小体的激活。细胞焦亡过程中常伴有炎症反应的发生,而炎症小体则是细胞产生焦亡和炎症反应所必需的多聚体蛋白复合物,其主要功能是活化caspase-1,从而间接调控炎症因子白介素1(IL-1)和IL-18的表达和分泌。最近的研究表明,细胞焦亡和炎症小体在非酒精性脂肪肝病的发生发展中起重要作用。针对该领域的最新研究进行综述,以期为非酒精性脂肪肝的防治提供新的科学认识和信息。

English Abstract

张文杰, 孙迪阳, 王培. 炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制[J]. 药学实践与服务, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
引用本文: 张文杰, 孙迪阳, 王培. 炎症小体介导的细胞焦亡在非酒精性脂肪肝病中的作用及机制[J]. 药学实践与服务, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
ZHANG Wenjie, SUN Diyang, WANG Pei. The role and mechanism of inflammasome-associated pyroptosis in nonalcoholic fatty liver disease[J]. Journal of Pharmaceutical Practice and Service, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
Citation: ZHANG Wenjie, SUN Diyang, WANG Pei. The role and mechanism of inflammasome-associated pyroptosis in nonalcoholic fatty liver disease[J]. Journal of Pharmaceutical Practice and Service, 2020, 38(1): 9-13,41. doi: 10.3969/j.issn.1006-0111.201902051
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