PPARα alleviates iron overload‐induced ferroptosis in mouse liver

A

Serum ALT and AST levels were measured in 8‐week‐old WT, PPARα^−/− mice that fed a normal diet or a HID; n = 3–5 mice/group.

B–D

Hepatic MDA content (B), hepatic GSH content (C), hepatic Ptgs2 mRNA levels (D) were measured in the indicated mice. n = 3–5 mice/group.

E

Liver tissue was obtained from the indicated mice and then examined using transmission electron microscopy (Arrowheads indicate mitochondria). Scale bars are 1 μm and 5 μm. n = 4 biological replicates.

F

Serum ALT and AST levels were measured in 8‐week‐old PPARα^−/− mice that were fed a HID with or without Gpx4‐AAV treatment; n = 8 mice/group.

G, I

Hepatic MDA content (G), hepatic iron content (H), hepatic Ptgs2 mRNA levels (I) were measured in the indicated mice; n = 8 mice/group.

J

Measurement of intracellular ROS levels by fluorescent probe DCFH‐DA, and the fluorescence intensity of ROS was calculated. All scale bars are 20 μm. n = 3 biological replicates.

K

Kaplan–Meier curves with univariate analysis of overall survival based on the Gpx4‐AAV treatment. n = 5–9 mice/group.

Figure 4. PPARα deletion increases susceptibility to iron overload‐induced ferroptosis.