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Diabetes 54:778-784, 2005
© 2005 by the American Diabetes Association, Inc.

Absence of Heme Oxygenase-1 Exacerbates Myocardial Ischemia/Reperfusion Injury in Diabetic Mice

Xiaoli Liu1, Jiao Wei1, David H. Peng1, Matthew D. Layne1,2, and Shaw-Fang Yet1,2

1 Pulmonary and Critical Care Division, Brigham and Women’s Hospital, Boston, Massachusetts
2 Department of Medicine, Harvard Medical School, Boston, Massachusetts

Increased production of reactive oxygen species contributes to the etiology of diabetes complications. Pathophysiological stimuli that increase oxidative stress upregulate heme oxygenase (HO)-1, a cytoprotective heme–degrading enzyme. We hypothesized that HO-1 may be important in myocardial injury that is exacerbated by diabetes. To test this hypothesis, the left anterior descending coronary arteries of nondiabetic and diabetic wild-type (HO-1+/+) and HO-1 null (HO-1–/–) mice were ligated for 1 h followed by 24 h reperfusion. The absence of HO-1 significantly increased myocardial infarct size (36.4 ± 2.0 vs. 21.4 ± 1.8% in HO-1+/+ mice), while cardiac-specific overexpression of HO-1 protected against myocardial ischemic injury in diabetic mice. Despite similar high blood glucose levels, diabetic HO-1–/– mice had fourfold higher oxidative stress and larger infarcts (56.0 ± 2.8%) than diabetic HO-1+/+ mice (30.8 ± 6.1%). Moreover, hyperglycemia increased the mortality of HO-1–/– mice (31.3%) after ischemia/reperfusion injury, and 55% of diabetic HO-1–/– mice had mural thrombi in the left ventricles. The increased mortality of diabetic HO-1–/– mice may be in part due to formation of left ventricular mural thrombi. Our data demonstrate that the absence of HO-1 renders animals more susceptible to myocardial ischemia/reperfusion damage and diabetes worsens the injury.

Address correspondence and reprint requests to Shaw-Fang Yet, PhD, Pulmonary and Critical Care Division, Brigham and Women’s Hospital, 75 Francis St., Thorn 932A, Boston, MA 02115. E-mail: syet{at}rics.bwh.harvard.edu


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