The macrophage migration inhibitory factor protein superfamily in obesity and wound repair

被引:53
作者
Kim, Bong-Sung [1 ,2 ,3 ]
Pallua, Norbert [3 ]
Bernhagen, Juergen [2 ]
Bucala, Richard [1 ]
机构
[1] Yale Univ, Sch Med, Dept Med, New Haven, CT 06510 USA
[2] Rhein Westfal TH Aachen, Inst Biochem & Mol Cell Biol, Aachen, Germany
[3] Rhein Westfal TH Aachen, Fac Med, Burn Ctr, Dept Plast & Reconstruct Surg Hand Surg, Aachen, Germany
关键词
D-DOPACHROME TAUTOMERASE; HUMAN ADIPOSE-TISSUE; FACTOR MIF; ADIPOCYTE SIZE; MESSENGER-RNA; CHRONIC INFLAMMATION; LOCAL PROLIFERATION; GLUCOSE-HOMEOSTASIS; INSULIN-RESISTANCE; MONONUCLEAR-CELLS;
D O I
10.1038/emm.2015.26
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The rising number of obese individuals has become a major burden to the healthcare systems worldwide. Obesity includes not only the increase of adipose tissue mass but importantly also the altered cellular functions that collectively lead to a chronic state of adipose tissue inflammation, insulin resistance and impaired wound healing. Adipose tissue undergoing chronic inflammation shows altered cytokine expression and an accumulation of adipose tissue macrophages (ATM). The macrophage migration inhibitory factor (MIF) superfamily consists of MIF and the recently identified homolog D-dopachrome tautomerase (D-DT or MIF-2). MIF and D-DT, which both bind to the CD74/CD44 receptor complex, are differentially expressed in adipose tissue and have distinct roles in adipogenesis. MIF positively correlates with obesity as well as insulin resistance and contributes to adipose tissue inflammation by modulating ATM functions. D-DT, however, is negatively correlated with obesity and reverses glucose intolerance. In this review, their respective roles in adipose tissue homeostasis, adipose tissue inflammation, insulin resistance and impaired wound healing will be reviewed.
引用
收藏
页码:e161 / e161
页数:10
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