细胞焦亡在肝脏疾病发生中作用的研究进展
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摘要
细胞焦亡是依赖于caspase-1和/或caspase-11,并伴有大量炎性因子释放的新型细胞程序性死亡。外界刺激通过信号通路作用于不同炎症小体,进而激活caspase-1和/或caspase-11,介导细胞渗透性肿胀破裂,形成细胞膜小孔,释放大量炎性因子,诱导细胞死亡。在肝纤维化、病毒性肝炎等多种肝脏疾病中细胞焦亡增强,而肝癌组织中细胞焦亡被抑制。本文就细胞焦亡的机制以及在肝硬化、病毒性肝炎、酒精性肝病、非酒精性脂肪性肝病、肝细胞癌发生、发展中作用的研究进展作一综述。
Pyroptosis is a novel programmed cell death depending on caspase-1/caspase-11 and is accompanied by the release of a large number of inflammatory cytokines. External stimuli act on differential inflammatory cells through signaling pathways, which activates caspase-1/caspase-11, intermediates osmotic swell and disruption of cells, forms small pores in the cell membrane, and induces cell death by releasing a large number of inflammatory factors. Pyroptosis is enhanced in liver fibrosis, viral hepatitis and other liver diseases, while it is inhibited in liver cancer tissue. This paper reviews the research progress of the mechanism of pyroptosis as well as its role in the development of liver diseases as cirrhosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease and hepatocellular carcinoma.
Pyroptosis is a novel programmed cell death depending on caspase-1/caspase-11 and is accompanied by the release of a large number of inflammatory cytokines. External stimuli act on differential inflammatory cells through signaling pathways, which activates caspase-1/caspase-11, intermediates osmotic swell and disruption of cells, forms small pores in the cell membrane, and induces cell death by releasing a large number of inflammatory factors. Pyroptosis is enhanced in liver fibrosis, viral hepatitis and other liver diseases, while it is inhibited in liver cancer tissue. This paper reviews the research progress of the mechanism of pyroptosis as well as its role in the development of liver diseases as cirrhosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease and hepatocellular carcinoma.
引文
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[19] NJEI B,ROTMAN Y,DITAH I,et al.Emerging trends in hepatocellular carcinoma incidence and mortality[J].Hepatology,2015,61(1):191-199.
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[21] BAO J,LU Y,DENG Y,et al.Association between IL-18 polymorphisms,serum levels,and HBV-related hepatocellular carcinoma in a Chinese population:a retrospective case-control study[J].Cancer Cell Int,2015,15(1):72-79.
[22] MA X,GUO P,QIU Y,et al.Loss of AIM2 expression promotes hepatocarcinoma progression through activation of mTOR-S6K1 pathway[J].Oncotarget,2016,7(24):36185-36197.
[23] WEI Q,MU K,LI T,et al.Deregulation of the NLRP3 inflammasome in hepatic parenchymal cells during liver cancer progression[J].Lab Invest,2014,94(1):52-62.
[24] WEI Q,GUO P,MU K,et al.Estrogen suppresses hepatocellular carcinoma cells through ER beta-mediated upregulation of the NLRP3 inflammasome[J].Lab Invest,2015,95(7):804-816.
[25] GURUNG P,LUKENS J R,KANNEGANTI T D.Mitochondria:diversity in the regulation of the NLRP3 inflammasome[J].Trends Mol Med,2015,21(3):193-201.
[26] CHU Q,JIANG Y,ZHANG W,et al.Pyroptosis is involved in the pathogenesis of human hepatocellular carcinoma[J].Oncotarget,2016,7(51):84658-84665.
[2] UMMANNI R,LEHNIGK U,ZIMMERMANN U,et al.Immunohistochemical expression of caspase-1 and -9,uncleaved caspase-3 and -6,cleaved caspase-3 and -6 as well as Bcl-2 in benign epithelium and cancer of the prostate[J].Exp Ther Med,2010,1(1):47-52.
[3] SONOHARA F,INOKAWA Y,KANDA M,et al.Association of inflammasome components in background liver with poor prognosis after curatively-resected hepatocellular carcinoma[J].Anticancer Res,2017,37(1):293-300.
[4] 祁会丽,姚丽芬.细胞焦亡激活机制及相关疾病研究进展[J].中华实用诊断与治疗杂志,2016,30(5):417-419.
[5] YANG Y,JIANG G,ZHANG P,et al.Programmed cell death and its role in inflammation[J].Mil Med Res,2015,2:12.
[6] ACCARIAS S,LUGO-VILLARINO G,FOUCRAS G,et al.Pyroptosis of resident macrophages differentially orchestrates inflammatory responses to Staphylococcus aureus in resistant and susceptible mice[J].Eur J Immunol,2015,45(3):794-806.
[7] SHI J,ZHAO Y,WANG K,et al.Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J].Nature,2015,526(7575):660-665.
[8] LEBEAUPIN C,PROICS E,DE BIEVILLE C H,et al.ER stress induces NLRP3 inflammasome activation and hepatocyte death[J].Cell Death Dis,2015,6(9):e1879-1891.
[9] SZABO G,CSAK T.Inflammasomes in liver diseases[J].J Hepatol,2012,57(3):642-654.
[10] PETRASEK J,BALA 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.
[11] YU X,LAN P,HOU X,et al.HBV inhibits LPS-induced NLRP3 inflammasome activation and IL-1β production via suppressing the NF-κB pathway and ROS production[J].J Hepatol,2017,66(4):693-702.
[12] BEIER J I,BANALES J M.Pyroptosis:an inflammatory link between NAFLD and NASH with potential therapeutic implications[J].J Hepatol,2018,68(4):643-645.
[13] NAWAZ R,ZAHID S,IDREES M,et al.HCV-induced regulatory alterations of IL-1β,IL-6,TNF-α,and IFN-γ operative,leading liver en-route to non-alcoholic steatohepatitis[J].Inflamm Res,2017,66(6):477-486.
[14] KOFAHI H M,TAYLOR N G A,HIRASAWA K,et al.Hepatitis C virus infection of cultured human hepatoma cells causes apoptosis and pyroptosis in both infected and bystander cells[J].Sci Rep,2016,6:37433-37447.
[15] KHANOVA E,WU R,WANG W,et al.Pyroptosis by caspase-11/4-gasdermin-D pathway in alcoholic hepatitis[J].Hepatology,2018,67(5):1737-1753.
[16] 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,2017,68(4):773-782.
[17] MRIDHA A R,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.
[18] 乔菲,郝蕾,晁旭.细胞焦亡与癌症关系的研究进展[J].中华实用诊断与治疗杂志,2018,32(11):1132-1134.
[19] NJEI B,ROTMAN Y,DITAH I,et al.Emerging trends in hepatocellular carcinoma incidence and mortality[J].Hepatology,2015,61(1):191-199.
[20] 钟锋,王金重,郭永学,等.肝细胞性肝癌自发破裂出血56例临床分析[J].中华实用诊断与治疗杂志,2014,28(8):779-781.
[21] BAO J,LU Y,DENG Y,et al.Association between IL-18 polymorphisms,serum levels,and HBV-related hepatocellular carcinoma in a Chinese population:a retrospective case-control study[J].Cancer Cell Int,2015,15(1):72-79.
[22] MA X,GUO P,QIU Y,et al.Loss of AIM2 expression promotes hepatocarcinoma progression through activation of mTOR-S6K1 pathway[J].Oncotarget,2016,7(24):36185-36197.
[23] WEI Q,MU K,LI T,et al.Deregulation of the NLRP3 inflammasome in hepatic parenchymal cells during liver cancer progression[J].Lab Invest,2014,94(1):52-62.
[24] WEI Q,GUO P,MU K,et al.Estrogen suppresses hepatocellular carcinoma cells through ER beta-mediated upregulation of the NLRP3 inflammasome[J].Lab Invest,2015,95(7):804-816.
[25] GURUNG P,LUKENS J R,KANNEGANTI T D.Mitochondria:diversity in the regulation of the NLRP3 inflammasome[J].Trends Mol Med,2015,21(3):193-201.
[26] CHU Q,JIANG Y,ZHANG W,et al.Pyroptosis is involved in the pathogenesis of human hepatocellular carcinoma[J].Oncotarget,2016,7(51):84658-84665.
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