GATA2 deficiency exacerbates chronic liver injury via disrupting hepatocyte death-regeneration balance: Clinical, histopathological, and molecular evidence

Figure 9 Hepatocyte-specific Gata2 knockdown impairs hepatic stress adaptation and exacerbates triglyceride metabolic dysregulation in chronic liver injury mice. A: Hepatic malondialdehyde content; B: Glutathione levels; C: Oxidized glutathione levels; D: Electron transfer chain complex I activity; E: Triglyceride levels; F: Representative transmission electron microscope images showing ultrastructural morphology: Nucleus (N), mitochondria (M) with cristae disruption, dilated endoplasmic reticulum (ER), and lipid droplets (L); G: Analysis of endoplasmic reticulum stress-related protein expression; H: Western blot analysis of oxidative stress-related protein expression levels; I: Western blot analysis of triglyceride metabolism-related protein expression levels. ^cP < 0.05, ^dP < 0.01 vs chronic liver injury group (CCl₄). MDA: Malondialdehyde; GSH: Glutathione; GSSG: Oxidized glutathione; ETC-CI: Electron transfer chain complex I; TG: Triglyceride; p-MLKL: Phosphorylated mixed lineage kinase domain-like protein; MLKL: Mixed lineage kinase domain-like protein; HSP60: Heat shock protein 60; GRP78: Glucose-regulated protein 78; GPX4: Glutathione peroxidase 4; UCP2: Uncoupling protein 2; PPARα: Peroxisome proliferator-activated receptor alpha; MCAD: Medium chain acyl-CoA dehydrogenase.