Absence of Atg7 in the liver disturbed hepatic regeneration after liver injury.

摘要: Background and aims Autophagy is a critical process in cell survival the maintenance of homeostasis. However, implementation therapeutic approaches based on autophagy mechanisms after liver damage still challenging. Methods We used hepatospecific Atg7-deficient murine model to address this question. Results showed that proliferation regeneration capacity hepatocytes was impaired. On one hand, steady-state hyperproliferation. other external triggers such as partial hepatectomy (PHx) or transplantation did not induce hepatocellular repopulation. After PHx, hepatocyte strongly decreased, accompanied by high mortality. This increase mortality could be overcome pharmacological mTOR inhibition. In accordance with hypoproliferation damage, failed repopulate hepatic injury model. mice hypertrophy, transient cellular transaminase levels followed strong perisinusoidal/pericellular fibrosis age. Their elevated modified activity index (mHAI) almost exclusively due apoptosis without any inflammation. These parameters were associated variations triglyceride content compromised lipid droplet formation PHx. Mechanistically, we also observed modulation HGF, PAK4, NOTCH3 YES1, which are proteins involved cycle regulation. Conclusion demonstrated important role hepatocytes. causative relationship between triglycerides essential for promoting recovery. Finally, inhibition overcame impact deficiency prevented