Division of CKD Pathophysiology, the University of Tokyo Graduate School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Glycoconj J. 2021 Jun;38(3):341-346. doi: 10.1007/s10719-021-09989-5. Epub 2021 Mar 11.
Glycation of proteins is a non-enzymatic posttranslational modification. Such random modification often deranges the structure and function of a wide range of proteins, and in turn leads to cellular dysfunction and organ damage. Protein glycation is thus an important topic in understanding the molecular mechanisms of the development or progression of various kinds of diabetes-related diseases. Meanwhile, organelle stress, such as mitochondrial or endoplasmic reticulum (ER) damage, is a causal factor for cellular dysfunction. Under pathogenic conditions, mitochondrial stress and ER stress are induced by glycated proteins. Intensive research has revealed the molecular mechanism of how glycation contributes to cell fate via organelle stress. This article will summarize the most recent evidence on organelle stress and glycation in kidney disease, especially diabetic kidney disease (DKD) associated with high glycation status.
蛋白质的糖化作用是一种非酶促的翻译后修饰。这种随机修饰常常使广泛的蛋白质的结构和功能紊乱，进而导致细胞功能障碍和器官损伤。因此，蛋白质糖化作用是理解各种与糖尿病相关疾病发展或进展的分子机制的重要课题。同时，细胞器应激，如线粒体或内质网（ER）损伤，是细胞功能障碍的一个因果因素。在致病条件下，糖化蛋白诱导线粒体应激和 ER 应激。深入的研究揭示了糖化通过细胞器应激影响细胞命运的分子机制。本文将总结关于肾脏疾病（特别是与高糖化状态相关的糖尿病肾病（DKD））中细胞器应激和糖化作用的最新证据。
