促丝裂原激活蛋白激酶在牙髓干细胞向成牙本质细胞分化和牙髓损伤修复中的作用
Regulation of mitogen-activated protein kinase in the odontoblast differentiation of dental pulp stem cells and pulp injury and reparation

摘要： 通过诱导牙髓干细胞（DPSC）向成牙本质细胞方向分化，龋源性牙髓炎的治疗将不再局限于根管治疗这一临床选择，修复治疗也不再成为缺失牙治疗的唯一方案。促丝裂原激活蛋白激酶（MAPK），尤其是P38MAPK通过直接或间接磷酸化特定的转录因子，将细胞外刺激信号转导至细胞及其核内，从而引起一系列细胞生物学反应，如细胞增殖、分化、转化和程序性死亡。骨形态发生蛋白-2、矿物三氧化物聚合体和Biodentine皆可诱导DPSC向成牙本质细胞分化，而三者正是通过MAPK信号转导通路发挥作用的。在组织工程支架诱导DPSC分化过程中，支架材料通过激活P38MAPK信号转导通路促进了DPSC的分化。此外，MAPK信号转导通路参与牙髓损伤修复中DPSC的迁移、黏附和分化，参与牙髓损伤修复中牙本质的形成。由于MAPK信号转导通路在细胞增殖、分化和生存等过程中都起着十分关键的作用，因此，深入研究其反应分子、作用底物和作用机制有着重要的理论和临床意义。
Abstract: Several more alternatives can be offered for the treatment of carious pulp disease and restoration of lost teeth by inducing the odontoblast differentiation of dental pulp stem cell(DPSC). Mitogen-activated protein kinases(MAPK), specifically P38MAPK, are involved in various cellular functions, such as cell proliferation, differentiation, and apoptosis, by transducing extracellular signal to the cell and nucleus through transcription factor phosphorylation. In addition, bone morphogenetic protein-2, mineral trioxide aggregate, and biodentin can induce the odontoblast differentiation of DPSC by regulating MAPK signaling pathway and certain scaffolds in tissue engineering. Moreover, the MAPK signaling pathway performs an important function in the migration, adhesion, and differentiation of DPSC during dental pulp injury. Based on the key function of MAPK signaling pathway, further study on the molecule, substrate, and mechanisms is crucial.
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