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Journal of Diabetes Research
Volume 2016 (2016), Article ID 2543268, 11 pages
Review Article

The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes

1Department of Immunology, Medical School, Yangtze University, Jingzhou 434023, China
2Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA
3Department of Medicine, Hospital of Yangtze University, Jingzhou 434000, China

Received 15 July 2016; Revised 8 November 2016; Accepted 29 November 2016

Academic Editor: Konstantinos Kantartzis

Copyright © 2016 Yanan Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Significance. With an alarming increase in recent years, diabetes mellitus has become a global challenge. Despite advances in treatment of diabetes mellitus, currently, medications available are unable to control the progression of diabetes and its complications. Growing evidence suggests that inflammation is an important pathogenic mediator in the development of diabetes mellitus. The perspectives including suggestions for new therapies involving the shift from metabolic stress to inflammation should be taken into account. Critical Issues. High-mobility group box 1 (HMGB1), a nonhistone nuclear protein regulating gene expression, was rediscovered as an endogenous danger signal molecule to trigger inflammatory responses when released into extracellular milieu in the late 1990s. Given the similarities of inflammatory response in the development of T2D, we will discuss the potential implication of HMGB1 in the pathogenesis of T2D. Importantly, we will summarize and renovate the role of HMGB1 and HMGB1-mediated inflammatory pathways in adipose tissue inflammation, insulin resistance, and islet dysfunction. Future Directions. HMGB1 and its downstream receptors RAGE and TLRs may serve as potential antidiabetic targets. Current and forthcoming projects in this territory will pave the way for prospective approaches targeting the center of HMGB1-mediated inflammation to improve T2D and its complications.