Heterogeneous population of macrophages in the development of non-alcoholic fatty liver disease

被引:1
作者
Cho, Ye Eun
Kwon, Yong Seong
Hwang, Seonghwan [1 ]
机构
[1] Pusan Natl Univ, Coll Pharm, Dept Mfg Pharm, Busan, South Korea
关键词
Fatty liver; Non-alcoholic fatty liver disease (NAFLD); Non-alcoholic steatohepatitis (NASH); Inflammation; Macrophages; Chemokines; PROLIFERATOR-ACTIVATED RECEPTOR; INSULIN-RESISTANCE; KUPFFER CELLS; PPAR-GAMMA; STEATOHEPATITIS DEVELOPMENT; HEPATIC INFLAMMATION; OBETICHOLIC ACID; MOUSE MODEL; AGONIST; GALECTIN-3;
D O I
10.1016/j.livres.2022.06.001
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Non-alcoholic fatty liver disease (NAFLD) is characterized by a spectrum of hepatic diseases, including fatty liver, non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. NAFLD is a hepatic manifestation of metabolic syndrome and has become the leading cause of liver transplantation, necessitating an in-depth understanding of its underlying pathogenic mechanisms and the identification of viable drug targets. Although fatty liver is benign and does not exert marked liver damage or inflammation, NAFLD progression involves inflammatory processes facilitated by immune cells. Macrophages and monocytes constitute the pool of innate immune cells that contribute to NAFLD development in association with other cell types, such as neutrophils, T cells, and natural killer cells. The concept that macrophages contribute to the inflammatory processes in NAFLD development has long been debated; however, the remarkable advances in experimental techniques have rapidly uncovered new subpopulations of macrophages and monocytes, whose functions need to be comprehensively elucidated. The current review focuses on the recent expansion of our knowledge of the heterogeneous population of macrophages crucially involved in NAFLD development. In addition, the present paper discusses ongoing efforts to target macrophages and inflammatory processes to develop optimal therapeutic agents against non-alcoholic steatohepatitis. & COPY; 2022 The Third Affiliated Hospital of Sun Yat-sen University. Publishing services by Elsevier B. V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
引用
收藏
页码:16 / 25
页数:10
相关论文
共 137 条
[1]   The transcriptional PPARβ/δ network in human macrophages defines a unique agonist-induced activation state [J].
Adhikary, Till ;
Wortmann, Annika ;
Schumann, Tim ;
Finkernagel, Florian ;
Lieber, Sonja ;
Roth, Katrin ;
Toth, Philipp M. ;
Diederich, Wibke E. ;
Nist, Andrea ;
Stiewe, Thorsten ;
Kleinesudeik, Lara ;
Reinartz, Silke ;
Mueller-Bruesselbach, Sabine ;
Mueller, Rolf .
NUCLEIC ACIDS RESEARCH, 2015, 43 (10) :5033-5051
[2]   Review of galectin-3 inhibitors in the treatment of nonalcoholic steatohepatitis [J].
Al Attar, Atef ;
Antaramian, Ani ;
Noureddin, Mazen .
EXPERT REVIEW OF CLINICAL PHARMACOLOGY, 2021, 14 (04) :457-464
[3]   The Role of Tissue Macrophage-Mediated Inflammation on NAFLD Pathogenesis and Its Clinical Implications [J].
Alisi, Anna ;
Carpino, Guido ;
Oliveira, Felipe L. ;
Panera, Nadia ;
Nobili, Valerio ;
Gaudio, Eugenio .
MEDIATORS OF INFLAMMATION, 2017, 2017
[4]   Adipocyte Apoptosis, a Link between Obesity, Insulin Resistance, and Hepatic Steatosis [J].
Alkhouri, Naim ;
Gornicka, Agnieszka ;
Berk, Michael P. ;
Thapaliya, Samjhana ;
Dixon, Laura J. ;
Kashyap, Sangeeta ;
Schauer, Philip R. ;
Feldstein, Ariel E. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2010, 285 (05) :3428-3438
[5]   Pharmacological inhibition of the chemokine CCL2 (MCP-1) diminishes liver macrophage infiltration and steatohepatitis in chronic hepatic injury [J].
Baeck, Christer ;
Wehr, Alexander ;
Karlmark, Karlin Raja ;
Heymann, Felix ;
Vucur, Mihael ;
Gassler, Nikolaus ;
Huss, Sebastian ;
Klussmann, Sven ;
Eulberg, Dirk ;
Luedde, Tom ;
Trautwein, Christian ;
Tacke, Frank .
GUT, 2012, 61 (03) :416-426
[6]  
Benedict M, 2017, WORLD J HEPATOL, V9, P715, DOI 10.4254/wjh.v9.i16.715
[7]   Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis [J].
Biddinger, Sudha B. ;
Hernandez-Ono, Antonio ;
Rask-Madsen, Christian ;
Haas, Joel T. ;
Aleman, Jose O. ;
Suzuki, Ryo ;
Scapa, Erez F. ;
Agarwal, Chhavi ;
Carey, Martin C. ;
Stephanopoulos, Gregory ;
Cohen, David E. ;
King, George L. ;
Ginsberg, Henry N. ;
Kahn, C. Ronald .
CELL METABOLISM, 2008, 7 (02) :125-134
[8]   Adipose tissue macrophages induce hepatic neutrophil recruitment and macrophage accumulation in mice [J].
Bijnen, Mitchell ;
Josefs, Tatjana ;
Cuijpers, Ilona ;
Maalsen, Constantijn J. ;
van de Gaar, Jose ;
Vroomen, Maria ;
Wijnands, Erwin ;
Rensen, Sander S. ;
Greve, Jan Willem M. ;
Hofker, Marten H. ;
Biessen, Erik A. L. ;
Stehouwer, Coen D. A. ;
Schalkwijk, Casper G. ;
Wouters, Kristiaan .
GUT, 2018, 67 (07) :1317-1327
[9]   Understanding the Heterogeneity of Resident Liver Macrophages [J].
Bleriot, Camille ;
Ginhoux, Florent .
FRONTIERS IN IMMUNOLOGY, 2019, 10
[10]   Selective versus total insulin resistance: A pathogenic paradox [J].
Brown, Michael S. ;
Goldstein, Joseph L. .
CELL METABOLISM, 2008, 7 (02) :95-96