Mechanistic insights into hepatic cell type-specific contributions to acetaminophen-induced acute liver injury

Figure 3 Overview of hepatic cell-type-specific responses in acetaminophen-induced acute liver injury. This schematic depicts the coordinated actions of hepatic cell populations under both homeostatic conditions and following acetaminophen [N-acetyl-p-aminophenol (APAP)]-induced acute liver injury. An APAP overdose induces mitochondrial oxidative stress in hepatocytes, stimulates activation of hepatic stellate cells, elicits pro-inflammatory responses from Kupffer cells and monocyte-derived macrophages, and causes dysfunction of liver sinusoidal endothelial cells. The roles of adaptive immune cells, including T and B cells, are highlighted in the modulation of inflammation and tissue repair. This comprehensive illustration underlines the importance of multicellular dynamics governing both the progression and resolution phases of APAP-induced liver injury. APAP: N-acetyl-p-aminophenol (Acetaminophen); CCL2: Chemokine (C-C motif) ligand 2; HSCs: Hepatic stellate cells; IL: Interleukin; KCs: Kupffer cells; LSECs: Liver sinusoidal endothelial cells; ROS: Reactive oxygen species; TNF-α: Tumor necrosis factor-alpha; VWF: Von Willebrand factor. This figure was created using BioRender.