肝血窦内皮细胞在非酒精性脂肪性肝病发展中的作用

蒋钊; 阮柏

doi:10.3969/j.issn.1001-5256.2020.03.047

肝血窦内皮细胞在非酒精性脂肪性肝病发展中的作用

DOI: 10.3969/j.issn.1001-5256.2020.03.047

蒋钊,
阮柏

1. 空军军医大学基础医学院学员一大队
2. 空军军医大学航空航天临床医学中心
3. 西京医院肝胆胰脾外科

基金项目:

国家自然科学基金项目(81800533)；陕西省自然科学基础研究计划(2019JQ-015)；

详细信息

中图分类号: R575.5
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- 被引次数: 0
出版历程
- 收稿日期: 2019-10-21
- 出版日期: 2020-03-20

The role of liver sinusoidal endothelial cells in the progression of nonalcoholic fatty liver disease

Jiang Zhao,
Ruan Bo

1st Cadet Regiment,School of Basic Medical Sciences,Air Force Medical University

Research funding:

摘要

摘要: 非酒精性脂肪性肝病(NAFLD)是以肝脏脂肪变、炎症和纤维化为主要表现的临床代谢综合征,日渐成为严重影响公众健康的常见慢性肝病。肝血窦内皮细胞(LSEC)是肝脏组织特化的血管内皮细胞,作为一道重要的血管屏障,其对肝脏细胞吸收和代谢源自肠道血液中的营养与物质成分发挥重要调节作用。介绍了NAFLD发生发展进程中LSEC毛细血管化、血管功能障碍及其参与调控肝脏炎症、血管生成、肝纤维化的研究进展。
- 非酒精性脂肪性肝病 /
- 毛细血管 /
- 内皮细胞
Abstract: Nonalcoholic fatty liver disease( NAFLD) is a clinical metabolic syndrome characterized by hepatic steatosis,inflammation,and fibrosis and has become a common chronic liver disease with great impact on public health. Liver sinusoidal endothelial cells( LSECs) are specialized vascular endothelium of liver tissue,and as an important vascular barrier,LSECs play an important role in regulating the absorption and metabolism of nutrients and substances from the blood of the intestines in hepatocytes. This article reviews the research advances in LSEC capillarization,vascular dysfunction,and its involvement in the regulation of liver inflammation,angiogenesis,and liver fibrosis during the development and progression of NAFLD.
- non-alcoholic fatty liver disease /
- capillaries /
- endothelial cells

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参考文献(30)

[1] FRIEDMAN SL,NEUSCHWANDER-TETRI BA,RINELLA M,et al. Mechanisms of NAFLD development and therapeutic strategies[J]. Nat Med,2018,24(7):908-922.

[2] YOUNOSSI ZM. Non-alcoholic fatty liver disease-A global public health perspective[J]. J Hepatol,2019,70(3):531-544.

[3] ESTES C,RAZAVI H,LOOMBA R,et al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease[J]. Hepatology,2018,67(1):123-133.

[4] MARRA F,SVEGLIATI-BARONI G. Lipotoxicity and the gutliver axis in NASH pathogenesis[J]. J Hepatol,2018,68(2):280-295.

[5] POISSON J,LEMOINNE S,BOULANGER C,et al. Liver sinusoidal endothelial cells:Physiology and role in liver diseases[J]. J Hepatol,2017,66(1):212-227.

[6] BLOMHOFF R,DREVON CA,ESKILD W,et al. Clearance of acetyl low density lipoprotein by rat liver endothelial cells. Implications for hepatic cholesterol metabolism[J]. J Biol Chem,1984,259(14):8898-8903.

[7] MIYAO M,KOTANI H,ISHIDA T,et al. Pivotal role of liver sinusoidal endothelial cells in NAFLD/NASH progression[J].Lab Invest,2015,95(10):1130-1144.

[8] HAMMOUTENE A,RAUTOU PE. Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease[J]. J Hepatol,2019,70(6):1278-1291.

[9] FRANCQUE S,VERRIJKEN A,MERTENS I,et al. Noncirrhotic human nonalcoholic fatty liver disease induces portal hypertension in relation to the histological degree of steatosis[J]. Eur J Gastroenterol Hepatol,2010,22(12):1449-1457.

[10] SEIFALIAN AM,PIASECKI C,AGARWAL A,et al. The effect of graded steatosis on flow in the hepatic parenchymal microcirculation[J]. Transplantation,1999,68(6):780-784.

[11] IJAZ S,YANG W,WINSLET MC,et al. The role of nitric oxide in the modulation of hepatic microcirculation and tissue oxygenation in an experimental model of hepatic steatosis[J]. Microvasc Res,2005,70(3):129-136.

[12] GARCIA-LEZANA T,RAURELL I,BRAVO M,et al. Restoration of a healthy intestinal microbiota normalizes portal hypertension in a rat model of nonalcoholic steatohepatitis[J]. Hepatology,2018,67(4):1485-1498.

[13] GONZALEZ-PAREDES FJ,HERNANDEZ MG,MORALES AD,et al. Contribution of cyclooxygenase end products and oxidative stress to intrahepatic endothelial dysfunction in early non-alcoholic fatty liver disease[J]. PLo S One,2016,11(5):e156650.

[14] PASARIN M,LA MURA V,GRACIA-SANCHO J,et al. Sinusoidal endothelial dysfunction precedes inflammation and fibrosis in a model of NAFLD[J]. PLo S One,2012,7(4):e32785.

[15] TATEYA S,RIZZO NO,HANDA P,et al. Endothelial NO/cGMP/VASP signaling attenuates Kupffer cell activation and hepatic insulin resistance induced by high-fat feeding[J]. Diabetes,2011,60(11):2792-2801.

[16] SCHILD L,DOMBROWSKI F,LENDECKEL U,et al. Impairment of endothelial nitric oxide synthase causes abnormal fat and glycogen deposition in liver[J]. Biochim Biophys Acta,2008,1782(3):180-187.

[17] WINDER WW,HARDIE DG. Inactivation of acetyl-Co A carboxylase and activation of AMP-activated protein kinase in muscle during exercise[J]. Am J Physiol,1996,270(2 Pt1):e299-e304.

[18] ROEDIGER WE,HEMS R,WIGGINS D,et al. Inhibition of hepatocyte lipogenesis by nitric oxide donor:Could nitric oxide regulate lipid synthesis?[J]. IUBMB Life,2004,56(1):35-40.

[19] MASLAK E,ZABIELSKI P,KOCHAN K,et al. The liver-selective NO donor,V-PYRRO/NO,protects against liver steatosis and improves postprandial glucose tolerance in mice fed high fat diet[J]. Biochem Pharmacol,2015,93(3):389-400.

[20] KUS K,WALCZAK M,MASLAK E,et al. Hepatoselective Nitric Oxide(NO)donors,V-PYRRO/NO and V-PROLI/NO,in nonalcoholic fatty liver disease:A comparison of antisteatotic effects with the biotransformation and pharmacokinetics[J].Drug Metab Dispos,2015,43(7):1028-1036.

[21] WANG W,ZHAO C,ZHOU J,et al. Simvastatin ameliorates liver fibrosis via mediating nitric oxide synthase in rats with non-alcoholic steatohepatitis-related liver fibrosis[J]. PLo S One,2013,8(10):e76538.

[22] XIE G,WANG X,WANG L,et al. Role of differentiation of liver sinusoidal endothelial cells in progression and regression of hepatic fibrosis in rats[J]. Gastroenterology,2012,142(4):918-927.

[23] FONTANA L,EAGON JC,TRUJILLO ME,et al. Visceral fat adipokine secretion is associated with systemic inflammation in obese humans[J]. Diabetes,2007,56(4):1010-1013.

[24] COULON S,FRANCQUE S,COLLE I,et al. Evaluation of inflammatory and angiogenic factors in patients with non-alcoholic fatty liver disease[J]. Cytokine,2012,59(2):442-449.

[25] COULON S,LEGRY V,HEINDRYCKX F,et al. Role of vascular endothelial growth factor in the pathophysiology of nonalcoholic steatohepatitis in two rodent models[J]. Hepatology,2013,57(5):1793-1805.

[26] LEFERE S,van de VELDE F,HOORENS A,et al. Angiopoietin-2 promotes pathological angiogenesis and is a therapeutic target in murine nonalcoholic fatty liver disease[J]. Hepatology,2019,69(3):1087-1104.

[27] KITADE M,YOSHIJI H,KOJIMA H,et al. Neovascularization and oxidative stress in the progression of non-alcoholic steatohepatitis[J]. Mol Med Rep,2008,1(4):543-548.

[28] COULON S,HEINDRYCKX F,GEERTS A,et al. Angiogenesis in chronic liver disease and its complications[J]. Liver Int,2011,31(2):146-162.

[29] DELEVE LD. Liver sinusoidal endothelial cells in hepatic fibrosis[J]. Hepatology,2015,61(5):1740-1746.

[30] MATZ-SOJA M,GEBHARDT R. The many faces of Hedgehog signalling in the liver:Recent progress reveals striking cellular diversity and the importance of microenvironments[J]. J Hepatol,2014,61(6):1449-1450.

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