Recovered Hepatocytes Promote Macrophage Apoptosis Through CXCR4 After Acetaminophen-Induced Liver Injury in Mice.

ABSTRACT: Acetaminophen (APAP) overdose is the main cause of acute liver failure in Western countries. The mechanism of APAP hepatotoxicity is associated with centrilobular necrosis which initiates infiltration of neutrophils, monocytes, and other leukocytes to the area of necrosis. Although it has been recognized that this infiltration of immune cells plays a critical role in promoting liver repair, mechanism of immune cell clearance that is important for resolution of inflammation and the return to normal homeostasis are not well characterized. CXCR4 is a chemokine receptor expressed on hepatocytes as well as neutrophils, monocytes, and hematopoietic stem cells. CXCR4 function is dependent on its selective expression on different cell types and thus can vary depending on the pathophysiology. This

SUBMITTER: Nguyen NT 

PROVIDER: S-EPMC9333410 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature