基于PI3K/Akt信号通路探讨抑郁症发病机制的研究进展

Research Progress in Pathogenesis of Depression Based on PI3K/Akt Signaling Pathway

抑郁症是临床常见的、发病机制尚不明确的精神疾病。磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/Akt)信号通路具有细胞保护、调节细胞代谢和学习记忆等功能,可能在抑郁症发病过程中扮演重要角色。PI3K/Akt信号通路的改变对脑内脑源性神经营养因子、哺乳动物雷帕霉素靶蛋白、糖原合酶激酶-3β和叉头框转录因子均有影响,且激活PI3K/Akt信号通路可改变各抑郁症发病机制假说中致病蛋白的表达,从而减轻抑郁样行为。目前PI3K/Akt信号通路的作用机制已开展相关研究,但其对抑郁症的发病机制仍未明确,有待进一步研究。

Depression is a common psychiatric disease with unclear pathogenesis.The phosphatidylinositol-3-kinase/protein kinase B(PI3K/Akt)signal pathway has the functions of cell protection,regulation of cell metabolism,regulation of learning and memory,and may play an important role in the pathogenesis of depression.Changes in PI3K/Akt signal pathway affect brain-derived neurotrophic factor,mammalian rapamycin target,glycogen synthase kinase-3βand forkhead box transcription factors.Moreover,activation of PI3K/Akt signaling pathway can change the expression of pathogenic proteins in various pathogenesis hypotheses of depression,thereby alleviating depressive behaviors.The mechanism of PI3K/Akt signaling pathway has been studied,but its role in the pathogenesis of depression is still unclear and needs to be further studied.