Demirtas Levent, Guclu Aydin, Erdur Fatih Mehmet, Akbas Emin Murat, Ozcicek Adalet, Onk Didem, Turkmen Kultigin
Department of Internal Medicine, Erzincan University, Erzincan, Turkey.
Division of Nephrology, Kırsehir Training and Research Hospital, Kırsehir, Turkey.
Indian J Med Res. 2016 Oct;144(4):515-524. doi: 10.4103/0971-5916.200887.
The prevalence of diabetes mellitus (DM) is increasing secondary to increased consumption of food and decreased physical activity worldwide. Hyperglycaemia, insulin resistance and hypertrophy of pancreatic beta cells occur in the early phase of diabetes. However, with the progression of diabetes, dysfunction and loss of beta cells occur in both types 1 and 2 DM. Programmed cell death also named apoptosis is found to be associated with diabetes, and apoptosis of beta cells might be the main mechanism of relative insulin deficiency in DM. Autophagic cell death and apoptosis are not entirely distinct programmed cell death mechanisms and share many of the regulator proteins. These processes can occur in both physiologic and pathologic conditions including DM. Besides these two important pathways, endoplasmic reticulum (ER) also acts as a cell sensor to monitor and maintain cellular homeostasis. ER stress has been found to be associated with autophagy and apoptosis. This review was aimed to describe the interactions between apoptosis, autophagy and ER stress pathways in DM.
由于全球范围内食物摄入量增加和身体活动减少，糖尿病（DM）的患病率正在上升。高血糖、胰岛素抵抗和胰腺β细胞肥大发生在糖尿病的早期阶段。然而，随着糖尿病的进展，1型和2型糖尿病都会出现β细胞功能障碍和丧失。程序性细胞死亡也称为凋亡，被发现与糖尿病有关，β细胞凋亡可能是糖尿病中相对胰岛素缺乏的主要机制。自噬性细胞死亡和凋亡并非完全不同的程序性细胞死亡机制，它们共享许多调节蛋白。这些过程可发生在包括糖尿病在内的生理和病理状况中。除了这两条重要途径外，内质网（ER）还作为细胞传感器来监测和维持细胞内稳态。内质网应激已被发现与自噬和凋亡有关。本综述旨在描述糖尿病中凋亡、自噬和内质网应激途径之间的相互作用。
