晚期糖基化终末产物受体(receptor for advanced glycation end products,RAGE)是一种多配体的膜受体,与配体结合后可启动多条信号通路,引起细胞内氧化应激和炎症反应等,导致细胞功能紊乱。RAGE在糖尿病并发症、炎症、阿尔采末病和肿瘤...晚期糖基化终末产物受体(receptor for advanced glycation end products,RAGE)是一种多配体的膜受体,与配体结合后可启动多条信号通路,引起细胞内氧化应激和炎症反应等,导致细胞功能紊乱。RAGE在糖尿病并发症、炎症、阿尔采末病和肿瘤等疾病的发生和发展中起重要作用。应用可溶性RAGE(sRAGE)、抗RAGE抗体或干扰RAGE与配体结合的抑制剂阻断RAGE的活化,是防治上述疾病的新策略。该文对RAGE配体与疾病的关系和RAGE-配体激活的信号通路进行阐述,并对近年来关于RAGE抑制剂的研究进展进行总结。展开更多
The β-amyloid protein (Aβ) has long been considered to associate with Alzheimer’s disease (AD). In addition, groups of evidence show that the soluble intracellular Aβ plays an important role in the disease develop...The β-amyloid protein (Aβ) has long been considered to associate with Alzheimer’s disease (AD). In addition, groups of evidence show that the soluble intracellular Aβ plays an important role in the disease development. The mitochondrial dysfunction induced by Aβ accumulation is a main pathologic process in early stage of AD. Matured Aβ is imported into the mitochondria through an unclear route. Once inside the mitochondria, Aβ is able to interact with a number of targets, including amyloid-binding alcohol dehydrogenase (ABAD) and cyclophilin D (CypD), which is a component of the mitochondrial permeability transition pore. Interference with the normal functions of these proteins results in mitochondrial injury, such as energy dyshomeostasis, production of reactive oxygen species, membrane permeability alteration and so on. This review explores the Aβ generation and location in mitochondria. The mitochondrial injury induced by the interaction between Aβ and its targets are also discussed.展开更多
文摘晚期糖基化终末产物受体(receptor for advanced glycation end products,RAGE)是一种多配体的膜受体,与配体结合后可启动多条信号通路,引起细胞内氧化应激和炎症反应等,导致细胞功能紊乱。RAGE在糖尿病并发症、炎症、阿尔采末病和肿瘤等疾病的发生和发展中起重要作用。应用可溶性RAGE(sRAGE)、抗RAGE抗体或干扰RAGE与配体结合的抑制剂阻断RAGE的活化,是防治上述疾病的新策略。该文对RAGE配体与疾病的关系和RAGE-配体激活的信号通路进行阐述,并对近年来关于RAGE抑制剂的研究进展进行总结。
文摘The β-amyloid protein (Aβ) has long been considered to associate with Alzheimer’s disease (AD). In addition, groups of evidence show that the soluble intracellular Aβ plays an important role in the disease development. The mitochondrial dysfunction induced by Aβ accumulation is a main pathologic process in early stage of AD. Matured Aβ is imported into the mitochondria through an unclear route. Once inside the mitochondria, Aβ is able to interact with a number of targets, including amyloid-binding alcohol dehydrogenase (ABAD) and cyclophilin D (CypD), which is a component of the mitochondrial permeability transition pore. Interference with the normal functions of these proteins results in mitochondrial injury, such as energy dyshomeostasis, production of reactive oxygen species, membrane permeability alteration and so on. This review explores the Aβ generation and location in mitochondria. The mitochondrial injury induced by the interaction between Aβ and its targets are also discussed.
