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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Bax deficiency reduces infarct size and improves long-term function after myocardial infarction
E Hochhauser1, Y Cheporko, N Yasovich
1Department of Cardiothoracic Surgery, Felsenstein Medical Research Center, Rabin Medical Center, Petah Tikva, Israel. hochhaus@post.tau.ac.il
Cell Biochemistry and Biophysics
|April 5, 2007
Summary
Mice lacking the Bax gene showed reduced heart damage and better function after myocardial infarction (MI). Bax knockout hearts demonstrated smaller infarct size and improved cardiac performance following coronary artery occlusion.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Myocardial infarction (MI) leads to significant heart damage.
- The Bax gene's role in post-MI cardiac remodeling is not fully understood.
- Previous studies indicated cardioprotection in isolated Bax knockout hearts after ischemia/reperfusion injury.
Purpose of the Study:
- To investigate the effect of Bax gene knockout on myocardial infarction (MI) in vivo.
- To assess cardiac function, infarct size, and biochemical markers in Bax knockout mice post-MI.
Main Methods:
- Surgical ligation of the left anterior descending coronary artery (LAD) in homozygous Bax knockout (Bax(-/-)) and wild-type (Bax(+/+)) mice.
- Echocardiography to measure left-ventricular dimensions and fractional shortening at 28 days post-MI.
- Assessment of infarct size, serum creatine kinase and lactate dehydrogenase levels, and caspase 3 activity at various time points post-MI.
Main Results:
- Bax(-/-) mice exhibited significantly smaller increases in left-ventricular end-diastolic and end-systolic diameters compared to Bax(+/+) mice at 28 days post-MI.
- Fractional shortening was significantly higher, and infarct size was significantly smaller in Bax(-/-) mice (24% vs. 37%) at 28 days post-MI.
- Lower serum creatine kinase and lactate dehydrogenase release, and reduced caspase 3 activity were observed in Bax(-/-) mice 24 hours post-MI.
Conclusions:
- Bax knockout mice demonstrate reduced infarct size and improved myocardial function following permanent coronary artery occlusion.
- The Bax gene plays a significant role in the cardiac response to myocardial infarction.
- Further investigation into the Bax gene's function in post-MI cardiac remodeling is warranted.
