Analyses of hepatocellular proliferation in a mouse model of α‐1‐antitrypsin deficiency
David A. Rudnick, Yunjun Liao, Jae‐Koo An, Louis J. Muglia, David H. Perlmutter, Jeffrey H. Teckman – 25 March 2004 – α‐1‐Antitrypsin (α1‐AT) deficiency is the most common cause of metabolic pediatric liver disease. Hepatocellular injury is caused by toxicity of the mutant α‐1‐antitrypsin Z (α1‐ATZ) molecule retained within hepatocytes. In these studies, we used the PiZ transgenic mouse model of α1‐AT deficiency to examine hepatocellular proliferation in response to chronic liver injury resulting from this metabolic disease.