创新链/学科链/研发链/产业链

新药研发前沿动态 / 医药领域趋势进展

铁死亡在非酒精性脂肪性肝炎发生发展中作用的研究进展

Research Progress on the Role of Ferroptosis in the Development of Non-alcoholic Steatohepatitis

  • 摘要: 铁死亡是铁依赖性的脂质过氧化物致死性堆积诱发的细胞死亡。胞内铁超载以及大量活性氧(ROS)积蓄催化细胞膜上高表达的不饱和脂肪酸过氧化,从而诱导细胞死亡。自噬、凋亡等细胞程序化死亡在非酒精性脂肪性肝炎(NASH)的发生发展中发挥关键作用。有研究发现铁死亡直接参与单纯性脂肪肝发展到NASH的进程,抑制铁死亡,几乎可以完全抑制NASH发生。通过对铁死亡是否参与NASH的进展进行综述,以期为NASH机制研究与临床治疗提供新的参考。

     

    Abstract: Ferroptosis refers to cell death induced by lethal accumulation of iron-dependent lipid peroxides. Intracellular iron overload and accumulation of a large amount of reactive oxygen species (ROS) catalyze the peroxidation of unsaturated fatty acids highly expressed on the cell membrane, thereby inducing cell death. Programmed cell death such as autophagy and apoptosis plays an important role in the occurrence and progression of non-alcoholic steatohepatitis (NASH). Research findings show that ferroptosis is directly involved in the development from simple fatty liver to NASH, inhibiting ferroptosis and almost completely inhibiting the occurrence of NASH. This review focuses on whether iron death is involved in the progression of NASH, which is expected to provide new reference for the mechanism research and clinical treatment of NASH.

     

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