PIM3 regulates myocardial ischemia/reperfusion injury via ferroptosis

Background Myocardial ischemia/reperfusion (I/R) injury is closely related with cardiovascular diseases; however, the underlying pathogenic mechanisms remain not fully understood. This study sought to investigate the effect and mechanisms of PIM3 implicated in myocardial I/R injury using a rat model...

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Published in:Genes & genomics 2024-02, Vol.46 (2), p.161-170
Main Authors: Li, Ting, Liu, Fangyao, Tan, Ying, Peng, Yutao, Xu, Xuefeng, Yang, Yushan
Format: Article
Language:English
Subjects:
Animal Genetics and Genomics
Animals
Biomedical and Life Sciences
Cardiovascular diseases
Cell survival
Cell viability
Cholecystokinin
Coronary Artery Disease
Cytology
Ferroptosis
Ferroptosis - genetics
Human Genetics
Iron
Ischemia
Life Sciences
Microbial Genetics and Genomics
Myocardial ischemia
Myocardial Reperfusion Injury - genetics
Plant Genetics and Genomics
Rats
Reactive Oxygen Species
Reperfusion
Research Article
Superoxide Dismutase
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Summary:Background Myocardial ischemia/reperfusion (I/R) injury is closely related with cardiovascular diseases; however, the underlying pathogenic mechanisms remain not fully understood. This study sought to investigate the effect and mechanisms of PIM3 implicated in myocardial I/R injury using a rat model of myocardial I/R injury and a cell model of oxygen–glucose deprivation/reoxygenation (OGD/R) induction. Methods The morphology changes were detected by HE staining while cell viability was accessed by the CCK-8 method. The characteristics of ferroptosis were evaluated by ROS production, MDA content, SOD level, iron content, TfR1, FTH1, and GPX4 expression. Results Myocardial I/R operation increased myocardial tissue damage in rats, while OGD/R treatment reduced the viability of H9c2 cells. Both myocardial I/R operation and OGD/R stimulation increased ferroptosis, as demonstrated by elevated ROS, MDA, iron content, decreased SOD level, upregulation of TfR1, and downregulation of FTH1 and GPX4. Additionally, myocardial I/R modeling or OGD/R treatment enhanced the expression of PIM3. Silencing of PIM3 inhibited ferroptosis, which resulted in alleviated myocardial I/R-induced damage and improved H9c2 cell survival. Conclusions Our findings highlight a vital role of PIM3 in myocardial I/R injury, indicating that PIM3-targeting ferroptosis may be a promising target for the development of novel therapies of myocardial I/R injury-associated diseases.
ISSN:1976-9571
2092-9293
2092-9293
DOI:10.1007/s13258-023-01475-6