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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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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