High mobility group box 1 (HMGB1) protein, in its role as a crucial injury-related molecule, displays a substantial correlation with the degree of liver steatosis.
HMGB1 >54 pg/ml (p=0.008, OR=6.05, CI=1.59-23.00) was significantly associated with the donor body mass index (p=0.008, OR=6.05, CI=1.59-23.00) and fatty liver (p=0.005, OR=11.68, CI=2.10-64.01).
In the cross-sectional analyses (n = 205 for PIVENS and 109 for TONIC), there was no significant relationship between serum HMGB1 levels and histological features such as steatosis, ballooning, inflammation, fibrosis, or presence of steatohepatitis in either adults or children.
We are the first to demonstrate that the SIRT1/HMGB1 pathway is a key therapeutic target for controlling NAFLD inflammation and that SalB confers protection against HFD- and PA-induced hepatic steatosis and inflammation through SIRT1-mediated HMGB1 deacetylation.