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

Figure 1 Hepatocellular mitochondrial injury and downstream death signaling triggered by acetaminophen overdose. Following acetaminophen overdose, N-acetyl-p-benzoquinone imine interacts with mitochondrial proteins, initiating oxidative stress and activation of phosphorylated c-Jun N-terminal kinase. These events induce mitochondrial permeability transition pore opening and result in the release of apoptosis-inducing factor and endonuclease G. Upon their translocation to the nucleus, these factors promote DNA fragmentation and necrotic cell death. AIF: Apoptosis-inducing factor; APAP: N-acetyl-p-aminophenol (Acetaminophen); JNK: C-Jun N-terminal kinase; MPT: Mitochondrial permeability transition; NAPQI: N-acetyl-p-benzoquinone imine; ROS: Reactive oxygen species. This figure was created using BioRender.