ArticleProceedings of the National Academy of Sciences of the United States of America2001
Gene program for cardiac cell survival induced by transient ischemia in conscious pigs.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 100 citations in OpenAlex.
- Heat shock protein 22: A new direction for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- Myocardial injury, troponin release, and cardiomyocyte death in brief ischemia, failure, and ventricular remodeling.American journal of physiology. Heart and circulatory physiology · 2022Review
- Heat Shock Protein 22 in Physiological and Pathological Hearts: Small Molecule, Large Potentials.Cells · 2021Review
- Insights of heat shock protein 22 in the cardiac protection against ischemic oxidative stress.Redox biology · 2020Review
- Secreted frizzled-related protein 2, a novel mechanism to induce myocardial ischemic protection through angiogenesis.Basic research in cardiology · 2020Article
- Review
- Redox Aspects of Chaperones in Cardiac Function.Frontiers in physiology · 2018Review
- Analysis of region specific gene expression patterns in the heart and systemic responses after experimental myocardial ischemia.Oncotarget · 2017Article
- Reply: Apoptosis, A Double-Edge Sword!JACC. Basic to translational science · 2017Article
- Tat-HSP22 inhibits oxidative stress-induced hippocampal neuronal cell death by regulation of the mitochondrial pathway.Molecular brain · 2017Article
- Multifunctional protein: cardiac ankyrin repeat protein.Journal of Zhejiang University. Science. B · 2016Review
- Article
- Molecular and cellular basis of viable dysfunctional myocardium.Circulation. Heart failure · 2014Review
- Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model.Neural regeneration research · 2013Article
- The valosin-containing protein promotes cardiac survival through the inducible isoform of nitric oxide synthase.Cardiovascular research · 2013Article
- Article
- Microarray analysis of differentially expressed background genes in rats following hemorrhagic shock.Molecular biology reports · 2012Article
- Effect of acute and chronic zofenopril administration on cardiac gene expression.Molecular and cellular biochemistry · 2011Article
- Preemptive conditioning of the swine heart by H11 kinase/Hsp22 provides cardiac protection through inducible nitric oxide synthase.American journal of physiology. Heart and circulatory physiology · 2011Article
- Hold me tight: Role of the heat shock protein family of chaperones in cardiac disease.Circulation · 2010Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Therapy for ischemic heart disease has been directed traditionally at limiting cell necrosis. We determined by genome profiling whether ischemic myocardium can trigger a genetic program promoting cardiac cell survival, which would be a novel and potentially equally important mechanism of salvage. Although cardiac genomics is usually performed in rodents, we used a swine model of ischemia/reperfusion followed by ventricular dysfunction (stunning), which more closely resembles clinical conditions. Gene expression profiles were compared by subtractive hybridization between ischemic and normal tissue of the same hearts. About one-third (23/74) of the nuclear-encoded genes that were up-regulated in ischemic myocardium participate in survival mechanisms (inhibition of apoptosis, cytoprotection, cell growth, and stimulation of translation). The specificity of this response was confirmed by Northern blot and quantitative PCR. Unexpectedly, this program also included genes not previously described in cardiomyocytes. Up-regulation of survival genes was more profound in subendocardium over subepicardium, reflecting that this response in stunned myocardium was proportional to the severity of the ischemic insult. Thus, in a swine model that recapitulates human heart disease, nonlethal ischemia activates a genomic program of cell survival that relates to the time course of myocardial stunning and differs transmurally in relation to ischemic stress, which induced the stunning. Understanding the genes up-regulated during myocardial stunning, including those not previously described in the heart, and developing strategies that activate this program may open new avenues for therapy in ischemic heart disease.
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