CAJ | 학술논문

糖尿病患者在血糖得到控制后,糖尿病并发症仍然持续发展的现象提示了以前暴露于高血糖导致的“代谢记忆”.近来的研究提示“代谢记忆”可能归因于靶细胞的表观遗传改变.许多实验证据显示:组蛋白乙酰基转移酶(HATs)、组蛋白去乙酰化酶(HDACs)、组蛋白甲基转移酶(HMTs)、组蛋白赖氨酸去甲基化酶(KDMs)以及microRNA在调节几种与糖尿病并发症相关的关键基因表观遗传修饰中发挥了重要作用.进一步阐明表观遗传修饰在糖尿病“代谢记忆”中的作用机制以及明确相应的细胞信号通路,对于糖尿病及其并发症的防治有重要意义.
당뇨병환자재혈당득도공제후,당뇨병병발증잉연지속발전적현상제시료이전폭로우고혈당도치적“대사기억”.근래적연구제시“대사기억”가능귀인우파세포적표관유전개변.허다실험증거현시:조단백을선기전이매(HATs)、조단백거을선화매(HDACs)、조단백갑기전이매(HMTs)、조단백뢰안산거갑기화매(KDMs)이급microRNA재조절궤충여당뇨병병발증상관적관건기인표관유전수식중발휘료중요작용.진일보천명표관유전수식재당뇨병“대사기억”중적작용궤제이급명학상응적세포신호통로,대우당뇨병급기병발증적방치유중요의의.
It is evident that metabolic memory,whereby diabetic complications continue to develop and progress in individuals who returned to normal glycemic control after a period of transient hyperglycemia,has long lasting effects.Recent studies suggest that “metabolic memory” may be due to epigenetic changes in target oells.Understanding the molecular changes in chromatin structure and the functional relationship with altered signaling pathways is now considered to represent an important conceptual challenge to explain diabetes and the phenomenon of metabolic memory.Emerging evidences indicate that critical gene-activating epigenetic changes may confer future cell memories. Many experimental evidences show that histone acetyltransferases (HATs), histone deacetylases (HDACs),histone methyltransferases (HMTs),histone lysine demethylases (KDMs),and microRNAs play important roles in the epigenetic changes of several key genes related to diabetic complications. Transient hyperglycemia promotes gene-activating epigenetic changes and signaling events critical in the development and progression of diabetic vascular complications.Further characterisation of these glucose-induced epigenetic events and the identification of key enzymes involved will help us to develop new therapeutic strategies for diabetes and its complications.