Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice.

ABSTRACT: Epidermal growth factor receptor (EGFR) is mostly known for its proliferative role in the liver. Our earlier investigations indicated a paradoxical cell-death-promoting facet of EGFR in the acetaminophen (APAP)-induced liver injury (AILI) model. The current study investigates this unexpected role of EGFR in promoting AILI using a hepatocyte-specific EGFR deletion mouse model. Hepatocyte-specific EGFR-deficient mice were generated by administering AAV8.TBG.Cre in EGFRfl/fl mice and were subsequently treated with a severely toxic dose (500 mg/kg) of APAP. Liver injury, regeneration, and associated signaling pathways were assessed at different time intervals. EGFR deletion did not alter early liver injury at 6 h but significantly attenuated the progression of liver injury at 12 and 24 h follo

SUBMITTER: Jain S 

PROVIDER: S-EPMC12614225 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature