Macrophage recruitment in obese adipose tissue

Obesity Reviews - Tập 16 Số 2 - Trang 127-136 - 2015
Yinglong Bai1,2, Qiang Sun1
1Division of Environmental Health Sciences, College of Public Health, Ohio State University, Columbus, Ohio, USA
2Molecular, Cellular, and Developmental Biology Program, College of Medicine, Ohio State University, Columbus, Ohio, USA

Tóm tắt

SummaryObesity is characterized as a chronic state of low‐grade inflammation with progressive immune cell infiltration into adipose tissues. Adipose tissue macrophages play critical roles in the establishment of the chronic inflammatory state and metabolic dysfunctions. The novel discovery that pro‐inflammatory macrophages are recruited to obese adipose tissue prompted an increased interest in the interplay between immune cells and metabolism. Since this discovery, many works have been published investigating the factors that lead to macrophage recruitment, the phenotypic change of adipose tissue macrophages, and metabolic dysfunctions. Adipokines and chemokines are key mediators that play crucial roles in crosstalk between adipocytes and macrophages and in regulating the adipose tissue inflammation. In the present review, we discuss the obesity‐mediated adipose tissue remodelling, and particularly, the role of adipokines/chemokines in macrophage recruitment to obese adipose tissue. This review provides new insights into the physiological role of these factors and identifies a potential therapeutic target for obesity and associated disorders.

Từ khóa


Tài liệu tham khảo

10.1038/nri2921

10.1172/JCI200319246

10.1172/JCI200319451

10.2337/db12-0868

10.2337/db11-0613

10.1161/ATVBAHA.108.170316

10.1126/science.1178331

10.1096/fj.04-2204com

10.1038/nm1185

10.1073/pnas.92.15.6957

10.1038/nature08991

10.1038/nature11464

10.1007/s00125-006-0335-z

10.1152/ajpendo.00549.2013

10.1371/journal.pone.0007250

10.1161/01.RES.0000163635.62927.34

10.1097/MCO.0b013e32833aabef

10.1016/B978-0-12-417028-5.00006-5

10.1002/path.4133

10.1038/ni.1937

10.1172/JCI29881

10.1194/jlr.M500294-JLR200

10.1128/IAI.73.4.1907-1916.2005

10.1155/2013/616193

10.1073/pnas.1300492110

10.2337/db07-0767

10.1172/JCI20514

10.1016/j.jtcvs.2008.08.022

10.1161/01.ATV.0000183883.72263.13

10.1016/j.molimm.2007.07.035

10.1074/jbc.M601284200

10.1210/jc.2007-2630

10.1093/eurheartj/ehn387

10.1126/science.7678183

10.1111/j.1365-2362.2004.01414.x

10.1210/jc.2008-0425

10.1159/000088261

10.1016/j.atherosclerosis.2013.01.024

10.1002/hep.23250

10.2337/db07-0360

10.1016/j.yexmp.2014.09.017

10.1038/nri1350

10.1038/nri1937

10.1210/en.2013-1607

10.2337/diabetes.53.5.1285

10.1530/JOE-11-0338

10.1038/oby.2010.84

10.1210/en.2013-2027

10.1530/eje.0.1480293

10.1097/00041433-200312000-00003

10.1161/01.CIR.103.8.1057

10.1210/en.2013-2011

10.1074/jbc.M109.088708

10.1126/science.1188280

10.1046/j.1432-1327.1999.00657.x

10.1016/S0167-4838(96)00227-0

10.1371/journal.pmed.0030287

10.1002/art.21518

10.1172/JCI200112455

10.2337/db07-0218

10.2337/db11-0832

10.1172/JCI42845

10.1074/jbc.M701831200

10.1126/scisignal.272re3

10.1016/j.cell.2010.07.041

10.2337/db09-0925

10.1038/nm.2851

10.1194/jlr.M200361-JLR200

10.1016/j.bbrc.2013.06.117

10.1074/jbc.M111.232975

10.1093/cvr/cvq360

10.1038/nm1168

10.4049/jimmunol.1103207

10.1089/wound.2012.0380

10.1016/j.vph.2009.12.004

10.1016/j.bbrc.2012.01.145

10.1210/jc.2005-0369

10.1038/nature05894

10.1016/j.cmet.2013.11.017

10.1172/JCI24335

10.1074/jbc.M804220200

10.1016/j.metabol.2013.06.008

10.2337/db07-0425

10.2337/db07-1061

10.1172/JCI26498

10.1152/ajprenal.00316.2013

10.1161/ATVBAHA.108.168633

10.1097/MOL.0b013e3283393867

10.1161/ATVBAHA.109.197442

10.2337/db11-1506

10.1089/jmf.2013.2912

10.1016/j.cmet.2009.03.002

10.1074/jbc.M109.018556

10.1016/S0083-6729(08)00605-5

10.1074/jbc.M700412200

10.1172/JCI15555

10.1038/oby.2012.7

10.1016/j.cell.2013.03.001

10.1016/j.bbi.2014.01.010