ArticleBasic research in cardiology2011
Gene transfer as a strategy to achieve permanent cardioprotection II: rAAV-mediated gene therapy with heme oxygenase-1 limits infarct size 1 year later without adverse functional consequences.
Article in Basic research in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Deficiency of heme oxygenase 1a causes detrimental effects on cardiac function.Journal of cellular and molecular medicine · 2024Article
- Counteraction of Myocardial Ferritin Heavy Chain Deficiency by Heme Oxygenase-1.International journal of molecular sciences · 2022Article
- Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure.Circulation · 2022Article
- Supplementation With Spirulina Reduces Infarct Size and Ameliorates Cardiac Function in a Pig Model of STEMI.Frontiers in pharmacology · 2022Article
- Effects of Heme Oxygenase-1 on c-Kit-Positive Cardiac Cells.International journal of molecular sciences · 2021Article
- HO-1 overexpression and underexpression: Clinical implications.Archives of biochemistry and biophysics · 2019Review
- Heme Oxygenases in Cardiovascular Health and Disease.Physiological reviews · 2016Review
- Heme Oxygenase-1 and Carbon Monoxide in the Heart: The Balancing Act Between Danger Signaling and Pro-Survival.Circulation research · 2016Review
- Translational Significance of Heme Oxygenase in Obesity and Metabolic Syndrome.Trends in pharmacological sciences · 2016Review
- Association of bilirubin with coronary artery calcification and cardiovascular events in the general population without known liver disease: the Heinz Nixdorf Recall study.Clinical research in cardiology : official journal of the German Cardiac Society · 2014Article
- Tongguan Capsule Protects against Myocardial Ischemia and Reperfusion Injury in Mice.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Therapeutic approaches to limit hemolysis-driven endothelial dysfunction: scavenging free heme to preserve vasculature homeostasis.Oxidative medicine and cellular longevity · 2013Review
- Genetic background, gender, age, body temperature, and arterial blood pH have a major impact on myocardial infarct size in the mouse and need to be carefully measured and/or taken into account: results of a comprehensive analysis of determinants of infarct size in 1,074 mice.Basic research in cardiology · 2012Article
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- Gene transfer of heme oxygenase-1 using an adeno-associated virus serotype 6 vector prolongs cardiac allograft survival.Journal of transplantation · 2012Article
- Article
- Gene transfer as a strategy to achieve permanent cardioprotection I: rAAV-mediated gene therapy with inducible nitric oxide synthase limits infarct size 1 year later without adverse functional consequences.Basic research in cardiology · 2011Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Extensive evidence indicates that heme oxygenase-1 (HO-1) exerts potent cytoprotective effects in response to stress. Previous studies have shown that gene therapy with HO-1 protects against myocardial ischemia/reperfusion injury for up to 8 weeks after gene transfer. However, the long-term effects of HO-1 gene therapy on myocardial ischemic injury and function are unknown. To address this issue, we created a recombinant adeno-associated viral vector carrying the HO-1 gene (rAAV/HO-1) that enables long-lasting transgene expression. Mice received injections in the anterior LV wall of rAAV/LacZ (LacZ group) or rAAV/HO-1 (HO-1 group); 1 year later, they were subjected to a 30-min coronary occlusion (O) and 4 h of reperfusion (R). Cardiac HO-1 gene expression was confirmed at 1 month and 1 year after gene transfer by immunoblotting and immunohistochemistry analyses. In the HO-1 group, infarct size (% of risk region) was dramatically reduced at 1 year after gene transfer (11.2 ± 2.1%, n = 12, vs. 44.7 ± 3.6%, n = 8, in the LacZ group; P < 0.05). The infarct-sparing effects of HO-1 gene therapy at 1 year were as powerful as those observed 24 h after ischemic PC (six 4-min O/4-min R cycles) (15.0 ± 1.7%, n = 10). There were no appreciable changes in LV fractional shortening, LV ejection fraction, or LV end-diastolic or end-systolic diameter at 1 year after HO-1 gene transfer as compared to the age-matched controls or with the LacZ group. Histology showed no inflammation in the myocardium 1 year after rAAV/HO-1-mediated gene transfer. These results demonstrate, for the first time, that rAAV-mediated HO-1 gene transfer confers long-term (1 year), possibly permanent, cardioprotection without adverse functional consequences, providing proof of principle for the concept of achieving prophylactic cardioprotection (i.e., "immunization against infarction").
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Registered trials
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