Fig. 2

MST1 deficiency disrupts hepatic cholesterol homeostasis, potentiates lipotoxic injury and inflammatory cascades, while activating cholesterol biosynthetic pathways. MST1-KO murine models subjected to 18-week NCD/WD dietary interventions exhibited: a serum lipid profile alterations including TC, LDL-cholesterol, and HDL-C concentrations. b Quantitative assessment of hepatic total and FC accumulation. c Histomorphometric characterization through Filipin-stained cholesterol visualization (100x), F4/80 + macrophage infiltration mapping, H&E-stained parenchymal architecture, and collagen deposition analysis via Masson’s trichrome (200x), with quantitative metrics for fluorescent intensity, inflammatory cell distribution, fibrotic content, and NAFLD pathological scoring. d Transcriptional activation patterns of inflammatory mediators and fibrogenesis markers in hepatic tissue. e Immunoblot analysis with densitometric quantification of SREBP2 proteolytic processing and MST1 expression in NCD-fed liver specimens. f mRNA profiling of cholesterol regulatory network components in NCD-treated hepatic samples. g Western blot densitometry illustrating SREBP2 maturation dynamics and MST1 levels in WD-exposed liver tissues. h WD-induced transcriptional reprogramming of cholesterol biosynthetic machinery components. Data expressed as mean ± SEM (n = 6/group) from triplicate experimental replicates* versus respective controls, with statistical significance denoted as *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001