Bax ablation protects against myocardial ischemiareperfusion injury in transgenic mice

Edith Hoehhauser, Shaye Kivity, Daniel Offen, Nilanjana Maulik, Hajime Otani, Yael Barhum, Hannah Pannet, Vladymir Shneyvays, Asher Shainberg, Valeri Goldshtaub, Anna Tobar, Bernardo A. Vidne

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194 Scopus citations


The role of the proapototic Bax gene in ischemia-reperfusion (I/R) injury was studied in three groups of mice: homozygotic knockout mice lacking the Bax gene (Bax-/-), heterozygotic mice (Bax+/-), and wild-type mice (Bax+/+). Isolated hearts were subjected to ischemia (30 min, 37°C) and then to 120 min of reperfusion. The left ventricular developed force of Bax-deficient vs. Bax+/+ hearts at stabilization and at 120 min of reperfusion was 1,411 ± 177 vs. 1,161 ± 137 mg and 485 ± 69 vs. 306 ± 68 mg, respectively. Superior cardiac function of Bax-/- hearts after I/R was accompanied by a decrease in creatine kinase release, caspase 3 activity, irreversible ischemic injury, and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelingpositive cardiomyocytes. Electron microscopic evaluation revealed reduced damage to mitochondria and the nuclear chromatin structure in Bax-deficient mice. In the Bax+/- hearts, the damage markers were moderate. The superior tolerance of Bax knockout hearts to I/R injury recommends this gene as a potential target for therapeutic intervention in patients with severe and intractable myocardial ischemia.

Original languageEnglish
Pages (from-to)H2351-H2359
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 53-6
StatePublished - 1 Jun 2003


  • Apoptosis
  • Bax-deficient hearts
  • Heart


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