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Updated: Dec 7, 2025
An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
Published on: July 14, 2023
Galectin-3 knock down inhibits cardiac ischemia-reperfusion injury through interacting with bcl-2 and modulating cell
Meiqi Zhang1, Kang Cheng1, Huan Chen2
1Department of Intensive Care Unit, Hangzhou Hospital of Traditional Chinese Medicine (Dingqiao District), Guangxing Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Abstract:
Acute myocardial infarction (AMI) is a fetal cardiovascular disease with high morbidity and mortality worldwide. In the present study, we elucidated the role of galectin-3 in preventing myocardial ischemic reperfusion injury. We found that galactin-3 was significantly up-regulated in the myocardium and cardiomyocyte subjected to ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) treatment, respectively. Galectin-3 knockdown significantly decreased the ischemic size of the left ventricular and the apoptosis of cardiomyocytes. Moreover, galectin-3 knockdown reversed the decrease of mitochondrial membrane potential and inhibited the inflammation response in myocardium and cultured cardiomyocyte induced by I/R and H/R, respectively. Further, this study revealed that galectin-3 interacted with bcl-2, instead of bax, in the cardiomyocyte, and regulated the phosphorylation of AKT, p70s6k, JNK, IκB and p65. Our findings demonstrated that galectin-3 could prevent myocardial I/R injury through interacting with bcl-2.
Insights
Galectin-3 protects against heart attack injury by interacting with bcl-2. Reducing galectin-3 levels lessened heart damage and cell death after ischemia/reperfusion.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Acute myocardial infarction (AMI) poses a significant global health burden due to high morbidity and mortality.
- Understanding the molecular mechanisms underlying myocardial ischemic reperfusion injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of galectin-3 in preventing myocardial ischemic reperfusion (I/R) injury.
- To elucidate the molecular interactions and signaling pathways modulated by galectin-3 during I/R.
Main Methods:
- Galectin-3 expression was analyzed in myocardial and cardiomyocyte models of ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R).
- Galectin-3 knockdown was performed to assess its impact on infarct size, cardiomyocyte apoptosis, mitochondrial membrane potential, and inflammatory responses.
- Protein-protein interactions (galectin-3 with bcl-2 and bax) and signaling pathway phosphorylation (AKT, p70s6k, JNK, IκB, p65) were examined.
Main Results:
- Galectin-3 was significantly upregulated in response to I/R and H/R.
- Knockdown of galectin-3 reduced infarct size, cardiomyocyte apoptosis, and inflammation, while restoring mitochondrial membrane potential.
- Galectin-3 was found to interact with bcl-2, not bax, and modulated key signaling pathways including AKT, p70s6k, JNK, IκB, and p65.
Conclusions:
- Galectin-3 plays a critical protective role in mitigating myocardial I/R injury.
- The protective effects of galectin-3 involve its interaction with bcl-2 and regulation of specific intracellular signaling pathways.
