自噬与p62/SQSTM1在肝缺血再灌注中的作用

自噬是溶酶体依赖性的降解系统，p62 作为重要的蛋白载体，可促进受损蛋白经蛋白酶体和自噬体清除。p62 在线粒体自噬等选择性自噬中发挥重要作用。p62 与 Keap1 结合并通过自噬清除 Keap1，这导致游离的 Nrf2 水平增加，而 Nrf2 又可促进 p62 表达。因此自噬、p62、Nrf2 三者间存在密切的联系，相互调控。同时，Nrf2 还可促进谷胱甘肽 (Glutathione, GSH)和硫氧还蛋白(Thioredoxin, TXN)等多种分子的表达，而在肝缺血再灌注损伤过程中，肝细胞内这些分子可能参与细胞死亡的过程。因此，自噬与 p62 在肝缺血再灌注中的具体机制仍需进一步研究明确。

Roles of autophagy and p62 /SQSTM1 in hepatic ischemia-reperfusion

Autophagy is a lysosomal dependent degradation system, and p62 itself is an important protein carrier to facilitate the removal of damaged proteins by proteasomes and autophagosomes. p62 plays an important role in selective autophagy such as mitochondrial autophagy. p62 binds to Keap1 and clears Keap1 through autophagy, leading to increased levels of free Nrf2. Nrf2 can promote the expression of p62, glutathione (GSH) and thioredoxin (TXN). Therefore, autophagy, p62 and Nrf2 are closely related and mutually regulated. However, in the process of hepatic ischemia-reperfusion injury, these molecules in hepatocytes may participate in the process of cell death, and the specific mechanism still needs to be further studied.