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PIM3 regulates myocardial ischemia/reperfusion injury via ferroptosis
Ting Li1, Fangyao Liu2, Ying Tan1
1Department of Cardiovascular Medicine, The First Affiliated Hosptal, University of South China, Hengyang, 421001, Hunan, People's Republic of China.
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.
Insights
PIM3 promotes ferroptosis in myocardial ischemia/reperfusion (I/R) injury. Targeting PIM3 and ferroptosis may offer new therapies for cardiovascular diseases linked to I/R injury.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Molecular Medicine
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a significant factor in cardiovascular diseases, but its mechanisms are not fully understood.
- Investigating novel molecular pathways involved in I/R injury is crucial for developing effective treatments.
Purpose of the Study:
- To explore the role and mechanisms of PIM3 in myocardial I/R injury.
- To determine if PIM3 influences ferroptosis during I/R injury.
Main Methods:
- Utilized a rat model for myocardial I/R injury and a cell model (H9c2) for oxygen-glucose deprivation/reoxygenation (OGD/R).
- Assessed tissue damage via HE staining and cell viability using CCK-8.
- Evaluated ferroptosis markers including reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), iron content, and key proteins (TfR1, FTH1, GPX4).
Main Results:
- Myocardial I/R and OGD/R treatments induced significant ferroptosis, evidenced by altered ROS, MDA, SOD, iron levels, and protein expressions.
- PIM3 expression was upregulated following I/R and OGD/R.
- Silencing PIM3 reduced ferroptosis, alleviated myocardial damage, and improved cell survival.
Conclusions:
- PIM3 plays a critical role in mediating ferroptosis in myocardial I/R injury.
- Targeting PIM3-induced ferroptosis presents a potential therapeutic strategy for I/R injury-associated cardiovascular diseases.
