Xu Jiancheng, Zhou Qi, Xu Wei, Cai Lu
Department of Clinical Laboratory at the First Bethune Hospital, Jilin University, Changchun 130021, China.
Exp Diabetes Res. 2012;2012:827971. doi: 10.1155/2012/827971. Epub 2011 Nov 24.
The endoplasmic reticulum (ER) is an organelle entrusted with lipid synthesis, calcium homeostasis, protein folding, and maturation. Perturbation of ER-associated functions results in an evolutionarily conserved cell stress response, the unfolded protein response (UPR) that is also called ER stress. ER stress is aimed initially at compensating for damage but can eventually trigger cell death if ER stress is excessive or prolonged. Now the ER stress has been associated with numerous diseases. For instance, our recent studies have demonstrated the important role of ER stress in diabetes-induced cardiac cell death. It is known that apoptosis has been considered to play a critical role in diabetic cardiomyopathy. Therefore, this paper will summarize the information from the literature and our own studies to focus on the pathological role of ER stress in the development of diabetic cardiomyopathy. Improved understanding of the molecular mechanisms underlying UPR activation and ER-initiated apoptosis in diabetic cardiomyopathy will provide us with new targets for drug discovery and therapeutic intervention.
内质网（ER）是一种负责脂质合成、钙稳态、蛋白质折叠和成熟的细胞器。内质网相关功能的紊乱会导致一种进化上保守的细胞应激反应，即未折叠蛋白反应（UPR），也称为内质网应激。内质网应激最初旨在补偿损伤，但如果内质网应激过度或持续时间过长，最终可能引发细胞死亡。现在内质网应激已与多种疾病相关。例如，我们最近的研究表明内质网应激在糖尿病诱导的心肌细胞死亡中起重要作用。众所周知，细胞凋亡被认为在糖尿病心肌病中起关键作用。因此，本文将总结文献和我们自己研究中的信息，重点关注内质网应激在糖尿病心肌病发展中的病理作用。更好地理解糖尿病心肌病中UPR激活和内质网引发的细胞凋亡的分子机制将为我们提供药物发现和治疗干预的新靶点。
