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2型糖尿病病变中由人类胰岛淀粉样多肽(hIAPP)形成的蛋白纤维沉淀被认为是引起β细胞凋亡的重要原因。目前,hIAPP诱导β细胞凋亡的确切机制尚未完全明了,很多研究显示hIAPP引起的β细胞膜破裂是hIAPP产生细胞毒性的主要原因。不仅hIAPP具有引起膜损伤,从而导致细胞淀粉样改变的细胞毒性机制,一些与错误折叠疾病(如阿尔兹海默病、帕金森综合征、朊病毒病等)相关的多肽和蛋白质也具有相同的细胞毒性机理。结合最新研究进展,讨论了hIAPP与膜的相互作用,阐述了hIAPP诱导β细胞凋亡的几种可能机制。
Precipitation of protein fibers from human islet amyloid polypeptide (hIAPP) in type 2 diabetic lesions is thought to be an important cause of beta-cell apoptosis. At present, the exact mechanism by which hIAPP induces β-cell apoptosis is not fully understood. Many studies have shown that hIAPP-induced β-cell membrane rupture is the major cause of hIAPP-induced cytotoxicity. Not only does hIAPP have a cytotoxic mechanism that causes membrane damage leading to amyloid changes in cells, some of the polypeptides and proteins associated with misfolded diseases (such as Alzheimer’s disease, Parkinson’s disease, prion diseases, etc.) also have the same Cytotoxicity mechanism. Combined with the latest research progress, the interaction between hIAPP and membrane was discussed, and several possible mechanisms by which hIAPP induced β-cell apoptosis were described.