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. 2022 Feb 2;10:672391. doi: 10.3389/fcell.2022.672391

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Copyright © 2022 Sun, Wu, Yu, Zhang, Shen, Chen, Tong, Fan, Shi and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ACSL4–LPCAT3–mediated ferroptosis was induced in the MI/R model. (A) Representative H&E-stained images of the myocardium of sham or MI/R-injured rats. Bar = 200 µm. (B) TTC-stained infarct area. (C,D) Expression of myocardial enzyme leakage indicators, such as LDH and CK-MB, measured using ELISAs. (E–H) Measurement of echocardiography. (I) Level of ROS in myocardial tissues. (J) Concentration of iron in tissues measured using iron assays. (K) Representative blots and analyses of ferroptosis-related markers, including GPX4, FTH1, ACSL4, LPCAT3, PTGS2, NRF2 (phosphorylated), and HIF, in myocardial tissues from sham or injured rats. (L) Real-time PCR analysis of gene expression in rats subjected to MI/R surgery. Data represent mean ± SD (n = 3 per group). ^* p < 0.05, ^** p < 0.01, ^*** p < 0.001 vs. the sham group.