糖尿病
氧化应激
神经退行性变
糖化血红素
糖尿病肾病
疾病
生物信息学
人口
医学
免疫抑制
肾脏疾病
内分泌学
透析
内科学
足细胞
肾病
生物
淀粉样蛋白(真菌学)
肾
药理学
泌尿系统
达帕格列嗪
线粒体
蛋白尿
神经认知
糖尿病前期
胰岛素
横纹肌溶解症
胰岛素抵抗
作者
Si Sun,Fangzhen Tian,Huanhuan Qiao,Qi Xin,Xinxu Zhang,Xinxu Zhang,Nan Song,Yuxing Yan,Ling Liu,Yili Wang,Lijie Zhang,Ke Chen,J L Yang,Shu Zhang,Jianning Zhang,Yonghui Li,Hao Wang,Xiao‐Dong Zhang,Xiao‐Dong Zhang
标识
DOI:10.1002/adma.202518331
摘要
ABSTRACT Type 2 diabetes mellitus is the most prevalent disease in the world, with one‐tenth of the population suffering from the disease, and the most critical challenges are its complications that induce high disability and mortality rates. The state‐of‐the‐art therapeutic agents can manage glucose but fail to prevent renal failure as well as neurodegeneration with immunosuppression. Herein, we developed a deep learning design strategy that exploits the ‘size‐fitting effect’ to engineer an atomic‐precision metal cluster for preventing diabetic complications by targeting metabolic abnormality and immunosuppression. The designed AuZn cluster achieves almost 100% α‐amylase inhibition and 88% α‐glucosidase inhibition, resulting in the normalized glycated hemoglobin and sustained glucose control. The intrinsic redox properties reduce oxidative stress damage, promoting β‐cell regeneration and metabolic stress alleviation. Consequently, the renal function, the most prevalent complications, shows that glomerular filtration can be restored to normal levels without urinary protein, while the clinical dulaglutide is not show any improvement. The key marker during early neurocognitive disorders, the amyloid precursor protein (APP) induced by complications, can be effectively suppressed, and diabetes induced organelle degeneration in neurons can be restored.
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