OPTN as a therapeutic target for acetaminophen-induced liver injury by activating mitophagy

Acetaminophen (APAP) is a leading cause of acute liver failure in Western countries result from the accumulation of damaged mitochondria. However, there is no related clinically useful therapeutic intervention. Optineurin (OPTN) is a multifunctional protein involved in autophagy, oxidative stress, as well as nuclear factor κB (NF-κB) and IRF3 signaling, and OPTN mutations are associated with several human diseases.Here, to study the role of OPTN in APAP induced liver injury, we performed RNA-seq analysis of isolated control and Optn-/- mouse liver tissues. RNA-seq analysis was performed on a total of 6 samples extracted from murine liver, post hepatic injury induced by acetaminophen administration. Transcriptional profiles were from replicate samples generated at 6 hours post injury. Replicate samples were generated from 2 individual animals sacrificed at each timepoint, and compared to a control of 2 animals not subjected to acetaminophen treatment.