摘要
PI3K/AKT信号通路可以通过调控基因表达,从而在细胞的存活、分化、生长、运动和凋亡等多种生理和病理过程中起到重要作用。尤其在肝纤维化的进展中,此信号通路发挥了重要的调节作用。本文将对目前有关PI3K/AKT信号通路在参与肝纤维化形成中,如何调控细胞外基质的降解、影响HSC的活化及调节肝窦毛细血管化等作用机制作一综述。这些资料不仅可以揭示相关疾病条件下,多个细胞与信号因子之间复杂的相互作用机制,而且能够突出通过阻断PI3K/AKT信号通路可以保护和治疗肝纤维化这一潜在的临床意义。
The phosphatidylinositol 3-kinase（PI3K）/Akt intracellular signaling pathway plays important roles in both normal physiological and pathogenic processes by regulating the expression of genes involved in cell survival,differentiation,growth,movement,and apoptosis.In particular,the PI3K/Akt signaling pathway has been implicated in the development and progression of haptic fibrosis.In this review,we summarize the current knowledge of the mechanisms by which PI3K/Akt signal transduction regulates extracellular matrix degradation,hepatic stellate cell activation,and sinusoidal capillarization,all of which play important roles in the formation of hepatic fibrosis.This information not only reveals the complex interplay of mulitple cellular processes and signaling factors underlying the disease condition,but also highlights the potential therapeutic benefit of inhibiting the PI3K/AKT pathway to prevent and treat liver fibrosis.
出处
《临床肝胆病杂志》
CAS
2013年第5期389-392,396,共5页
Journal of Clinical Hepatology
基金
国家自然科学基金项目(81072803)
