Bax deficiency reduces infarct size and improves long-term function after myocardial infarction

E. Hochhauser, Y. Cheporko, N. Yasovich, L. Pinchas, D. Offen, Y. Barhum, H. Pannet, A. Tobar, B. A. Vidne, E. Birk

Research output: Contribution to journalArticlepeer-review


We have previously found that, following myocardial ischemia/reperfusion injury, isolated hearts from bax gene knockout mice [Bax(-/-)] exhibited higher cardioprotection than the wild-type. We here explore the effect of Bax(-/-), following myocardial infarction (MI) in vivo. Homozygotic Bax(-/-) and matched wild-type were studied. Mice underwent surgical ligation of the left anterior descending coronary artery (LAD). The progressive increase in left-ventricular end diastolic diameter, end systolic diameter, in Bax(-/-) was significantly smaller than in Bax(+/+) at 28 d following MI (p < 0.03) as seen by echocardiography. Concomitantly, fractional shortening was higher (35 ± 4.1% and 27 ± 2.5%, p < 0.001) and infarct size was smaller in Bax(-/-) compared to the wild-type at 28 days following MI (24 ± 3.7 % and 37 ± 3.3%, p < 0.001). Creatine kinase and lactate dehydrogenase release in serum were lower in Bax(-/-) than in Bax(+/+) 24 h following MI. Caspase 3 activity was elevated at 2 h after MI only in the wild-type, but reduced to baseline values at 1 and 28 d post-MI. Bax knockout mice hearts demonstrated reduced infarct size and improved myocardial function following permanent coronary artery occlusion. The Bax gene appears to play a significant role in the post-MI response that should be further investigated.

Original languageEnglish
Pages (from-to)11-19
Number of pages9
JournalCell Biochemistry and Biophysics
Issue number1
StatePublished - Jan 2007


  • Apoptosis
  • Bax-deficient hearts
  • Caspase
  • Myocardial infarction


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