Fig. 8: GP73 neutralization improves survival in ASGR1-deficient mice treated with APAP. | Nature Communications

Fig. 8: GP73 neutralization improves survival in ASGR1-deficient mice treated with APAP.

From: Deficiency of ASGR1 promotes liver injury by increasing GP73-mediated hepatic endoplasmic reticulum stress

Fig. 8: GP73 neutralization improves survival in ASGR1-deficient mice treated with APAP.

a Schematic diagram of mice treatment. 8-week-old Asgr1−/− and WT mice were intraperitoneally injected with anti-GP73 (10 mg/kg body weight) or IgG 10 hours after a lethal dose of APAP injection (650 mg/kg body weight). b Survival curves of mice treated with either IgG or anti-GP73 10 h after lethal APAP dosing (n = 20; WT+IgG vs. Asgr1−/−+IgG, P = 0.00034; WT+anti-GP73 vs. Asgr1−/−+anti-GP73, P = 0.5957). Data are presented as mean ± SEM. P values were calculated by Log-Rank test. **P < 0.01. c Working model of ASGR1 in liver injury. Left, in the presence of ASGR1, it binds to and mediates GP73 endocytosis and lysosomal degradation to maintain the homeostasis of circulating GP73 levels. Right, ASGR1 deficiency inhibits GP73 endocytosis and degradation, leading to excessive accumulation of GP73 in the circulation. As a result, the interaction between accumulated GP73 and BIP is enhanced, leading to increased ER stress and liver injury. Working model of ASGR1 in liver injury created with BioRender.com. Source data are provided as a Source Data file.

Back to article page