Transcriptomic signatures of p16-high (p16h) hepatocytes in CCl4-treated liver

The mechanisms by which aging promotes fibrotic processes remain to be elucidated. The preceding observation indicating a robust correlation between the severity of fibrosis in human cirrhotic patients and the population of hepatocytes expressing elevated levels of p16Ink4a (p16h), propose that p16h hepatocytes might serve as initiators of fibrogenic processes in response to liver injury. In this study, we employed a CCl4-induced hepatitis model to promote a fibrogenic process and observed the accumulation of p16h hepatocytes in zone 3.