Juwono Joshua, Martinus Ryan D
School of Science, University of Waikato, Private Bag 3105, Hamilton 3240, New Zealand.
J Diabetes Res. 2016;2016:8017571. doi: 10.1155/2016/8017571. Epub 2016 Jul 12.
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.
本综述的重点是总结热休克蛋白60(Hsp60)的表达及其与1型和2型糖尿病发病机制之间已知的关系。Hsp60是一种由线粒体损伤诱导产生的线粒体应激蛋白。已知它可从多种细胞类型中分泌出来,并且在1型和2型糖尿病患者中均已记录到其循环水平。然而,细胞外Hsp60的生物学意义仍有待确定。我们将研究Hsp60与细胞抗炎和促炎过程之间的联系,并具体探讨Hsp60如何通过至少两种不同机制影响免疫炎症:作为天然免疫受体的配体以及作为适应性免疫受体识别的抗原。我们还将研究Hsp60在动脉粥样硬化免疫细胞激活过程中的作用,动脉粥样硬化是糖尿病发病机制中的一个重要危险因素。