METTL3 deficiency aggravates hepatic ischemia/reperfusion injury in mice by activating the MAPK signaling pathway
Inflammatory responses, apoptosis, and oxidative stress, are key factors that contribute to hepatic ischemia/reperfusion (I/R) injury, which may lead to the failure of liver surgeries, such as hepatectomy and liver transplantation. The N6-methyladenosine (m6A) modification has been implicated in multiple biological processes, and its specific role and mechanism in hepatic I/R injury require further investigation. We found that METTL3 may be involved in regulating this process.  Therefore, we constructed an ischemia-reperfusion model with Hepatocyte-specific METTL3 knockdown (HKD) mice, and performed RNA- sequencing analysis with wild-type mice as controls. Overall design: Hepatocyte-specific METTL3 knockdown (METTL3-HKD) mice and METTL3-Flox mice were subjected to 1 h of ischemia and subsequent reperfusion for 6 h. Their livers were collected for RNA sequencing.