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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 eukaryotic organelle and is an important site for protein synthesis and secretion. When cells are stimulated to some extent by the outside world, ER produces a series of regulatory mechanisms to form endoplasmic reticulum stress (ERS). ERS causes misfolded and unfolded proteins in the ER lumen to aggregate, as well as Ca2 + imbalance. Activates the unfolded protein response (UPR) to protect cells from ERS-induced cell damage and restore cellular function. However, when the stress reaction is too strong or stimulus time is too long, it will induce apoptosis and cause disease. The formation of dental fluorosis is due to the synthesis of ameloblasts and hydrolytic protein dysfunction, therefore, infer the ERS and the occurrence of dental fluorosis. The mechanisms and pathways of ERS-induced apoptosis are summarized, and the role of this mechanism in the formation of dental fluorosis is reviewed.