The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes.
The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes.
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DOI：
10.1155/2016/2543268
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发表时间：
2016
影响因子：
4.3
通讯作者：
Ren B
中科院分区：
文献类型：
--
作者：
Wang Y;Zhong J;Zhang X;Liu Z;Yang Y;Gong Q;Ren B
意义随着近年来糖尿病的惊人增长，糖尿病已成为全球性挑战。尽管在糖尿病治疗方面取得了进展，但目前可用的药物无法控制糖尿病及其并发症的进展。越来越多的证据表明，炎症是糖尿病发展中的重要致病介质。应考虑包括涉及从代谢应激向炎症转变的新疗法建议在内的观点。关键问题。高迁移率族蛋白1（HMGB1）是一种调节基因表达的非组蛋白核蛋白，在20世纪90年代末被重新发现为内源性危险信号分子，当释放到细胞外环境时触发炎症反应。鉴于炎症反应在T2D发展中的相似性，我们将讨论HMGB1在T2D发病机制中的潜在意义。重要的是，我们将总结和更新HMGB1和HMGB1介导的炎症途径在脂肪组织炎症，胰岛素抵抗和胰岛功能障碍中的作用。未来的方向。HMGB1及其下游受体TLRs和TLR可能是潜在的抗糖尿病靶点。该领域目前和即将开展的项目将为针对HMGB1介导的炎症中心的前瞻性方法铺平道路，以改善T2D及其并发症。
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.
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影响因子：
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作者：
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影响因子：
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