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Review
. 2016:2016:3896147.
doi: 10.1155/2016/3896147. Epub 2016 Oct 25.

High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications

Han Wu  1 , Zheng Chen  1 , Jun Xie  1 , Li-Na Kang  1 , Lian Wang  1 , Biao Xu  1
Affiliations
Review

High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications

Han Wu et al. Mediators Inflamm. 2016.

Abstract

High mobility group box-1 (HMGB-1), a damage-associated molecular pattern, can be actively or passively released from various cells under different conditions and plays a pivotal role in the pathogenesis of inflammation and angiogenesis-dependent diseases. More and more evidence suggests that inflammation, in addition to its role in progression of diabetes, also promotes initiation and development of diabetic complications. In this review, we focus on the role of HMGB-1 in diabetes-related complications and the therapeutic strategies targeting HMGB-1 in diabetic complications.

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Figures

Figure 1
Figure 1
Schema depicting the structure of HMGB-1 and the molecular mechanisms responsible for the role of HMGB-1 in inflammation. (a) HMGB-1 translocates from the nucleus to the cytoplasm under oxidative stress condition and then is actively (immune or active inflammatory cells) or passively (death, apoptosis, or necrosis cells) released outside the cells. Once it is released into the extracellular space, HMGB-1 in turn promotes oxidative stress by binding to its receptors (such as RAGE, TLR2, and TLR4). (b) Extracellular HMGB-1 binds to its receptors and induces inflammatory response via various signaling pathways involving NF-κB, MyD88, p38MAPK, ERK, and JNK.
Figure 2
Figure 2
Schematic representation of HMGB-1-mediated cellular signaling pathways in islet cells.
See this image and copyright information in PMC

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