The Effect of Increased HSF1-HMOX1 Expression in H9C2 Cardiomyocytes Following Hypoxia/Reoxygenation on Myocardial Ferroptosis and M1 Polarization of Macrophages
Investigates the role of HSF1 and HMOX1 in ferroptosis and macrophage polarization in myocardial ischemia/reperfusion injury, highlighting potential therapeutic targets.
Key Points
This research aims to understand how the HSF1–HMOX1 interaction influences ferroptosis and myocardial injury during ischemia/reperfusion.
Established an ischemia/reperfusion rat model using coronary artery ligation
Conducted hypoxia/reoxygenation experiments on H9c2 cardiomyocytes
Performed HSF1 overexpression and knockdown manipulations
Assessed myocardial injury through CK-MB and cTn-I levels
Evaluated ferroptosis via ROS detection and protein assays
HSF1 and HMOX1 levels rose initially during I/R before decreasing after 24 hours
HSF1 overexpression increased ROS, leading to more ferroptosis
HSF1 knockdown reduced both ferroptosis and myocardial injury
HMOX1 knockdown countered the effects of HSF1 overexpression
The interaction between HSF1 and HMOX1 enhanced M1 macrophage polarization, increasing inflammatory cytokines like TNF-α and IL-6