Fig. 7: The interaction between TMEM16A and GPX4 is indispensable for TMEM16A function in hepatic I/R injury. | Cell Death & Disease

Fig. 7: The interaction between TMEM16A and GPX4 is indispensable for TMEM16A function in hepatic I/R injury.

From: Hepatocyte-specific TMEM16A deficiency alleviates hepatic ischemia/reperfusion injury via suppressing GPX4-mediated ferroptosis

Fig. 7

A Representative immunohistochemical staining of 4-HNE in liver sections of AAV-Con-, AAV-TM-, and AAV-TM-M-treated mice subjected to 90 min of hepatic ischemia followed by 24 h of reperfusion. Hepatic levels of B MDA, C PTGS2, and D serum iron content (n = 6). **P < 0.01 versus AAV-Con I/R; ##P < 0.01 versus AAV-TM I/R. E Representative H&E staining, necrotic area quantification, and Suzuki histological score in liver samples, and F serum ALT and AST levels in indicated mice followed by 90 min of ischemia and 24 h of reperfusion (n = 6–8). **P < 0.01 versus AAV-Con I/R; ##P < 0.01 versus AAV-TM I/R. G Western blot analysis and quantification of levels of hepatic GPX4 protein and proteins related to the NF-κB signaling pathway from the indicated groups (n = 6). *P < 0.05, **P < 0.01 versus AAV-Con I/R; ##P < 0.01 versus AAV-TM I/R. Data were presented as the mean ± SD.

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