内质网应激诱导细胞凋亡的机制及其在氟斑牙形成中的作用

The mechanism of apoptosis mediated by ERS and the role of ERS in the dental fluorosis

内质网(endoplasmic reticulum,ER)是一种重要的真核细胞器,是蛋白质合成与分泌的重要场所。当细胞受到外界的某些刺激时,ER会产生一系列调节机制,形成内质网应激(endoplasmic reticulum stress,ERS)。ERS使ER腔内错误折叠与未折叠蛋白聚集以及Ca2+平衡紊乱。可激活未折叠蛋白反应(unfolded protein response,UPR),以保护由ERS所引起的细胞损伤,恢复细胞功能。但当应激反应过强或刺激时间过长时,则会诱导细胞凋亡,引起疾病的发生。氟斑牙的形成是由于成釉细胞合成与水解蛋白质功能障碍,因此,推断ERS与氟斑牙的产生有关。现对ERS诱导细胞凋亡的机制和途径,以及这一机制在氟斑牙形成中的作用进行综述。

Endoplasmic reticulum （ER）is an important organelle of eukaryotic cells. ER will produce a series of regulato- ry mechanism under some stimulus, collectively called endoplasmic reticulum stress. Endoplasmic reticulum stress can accumulate unfolded or misfolded proteins in the ER, which affect the balance of Ca2＋. To resolve cellular damage, the ER triggers the unfolded protein response to maintain ER homeostasis .However, the apoptosis will occur with increasing stimulus and time of exposure .Too much apoptosis can also cause disease. Dental fluorosis is caused by inhibiting pro- tein secretion and/or synthesis, so we infer that endoplasmic reticulum stress may be responsible for dental fluorosis. This paper reviewed the mechanism of endoplasmic reticulum stress effects on cells, and their possible mechanisms of in- volvement in dental fluorosis.