Does Hsp60 Provide a Link between Mitochondrial Stress and Inflammation in Diabetes Mellitus?
Does Hsp60 Provide a Link between Mitochondrial Stress and Inflammation in Diabetes Mellitus?
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DOI：
10.1155/2016/8017571
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发表时间：
2016
影响因子：
4.3
通讯作者：
Martinus RD
中科院分区：
文献类型：
--
作者：
Juwono J;Martinus RD
本文就热休克蛋白60（Hsp60）的表达与1型和2型糖尿病发病机制的关系作一综述。Hsp60是一种由线粒体损伤诱导的线粒体应激蛋白。已知它由多种细胞类型分泌，并且在1型和2型糖尿病患者中均记录了循环水平。然而，细胞外Hsp60的生物学意义仍有待确定。我们将研究热休克蛋白60和细胞的抗炎和促炎过程之间的联系，并具体解决如何热休克蛋白60似乎影响免疫炎症至少有两种不同的机制：作为先天免疫受体的配体和作为抗原识别的适应性免疫受体。我们还将研究热休克蛋白60在免疫细胞激活过程中在动脉粥样硬化中的作用，动脉粥样硬化是糖尿病发病过程中的一个重要危险因素。
The focus of this review is to summarise the known relationships between the expression of heat shock protein 60 (Hsp60) and its association with the pathogenesis of Type 1 and Type 2 diabetes mellitus. Hsp60 is a mitochondrial stress protein that is induced by mitochondrial impairment. It is known to be secreted from a number of cell types and circulating levels have been documented in both Types 1 and 2 diabetes mellitus patients. The biological significance of extracellular Hsp60, however, remains to be established. We will examine the links between Hsp60 and cellular anti- and proinflammatory processes and specifically address how Hsp60 appears to affect immune inflammation by at least two different mechanisms: as a ligand for innate immune receptors and as an antigen recognised by adaptive immune receptors. We will also look at the role of Hsp60 during immune cell activation in atherosclerosis, a significant risk factor during the pathogenesis of diabetes mellitus.