ArticleInternational journal of medical sciences2012
Early biventricular molecular responses to an acute myocardial infarction.
Article in International journal of medical sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- SERPINB1 overexpression protects myocardial damage induced by acute myocardial infarction through AMPK/mTOR pathway.BMC cardiovascular disorders · 2022Article
- Hemodynamic Support Using Percutaneous Transfemoral Impella 5.0 and Impella RP for Refractory Cardiogenic Shock.Case reports in cardiology · 2019Article
- Differential gene expression profiles in peripheral blood in Northeast Chinese Han people with acute myocardial infarction.Genetics and molecular biologyArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose.
objectivesThe aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI. MATERIAL AND
methodsA rat model of left anterior descending coronary artery ligation was used to assess the effect of left ventricular AMI on both the right ventricle as a remote zone and the left ventricle as an ischemic/infarct zone. Microarray technology was applied to detect the gene expression. Gene Ontology and KEGG pathways analysis were done to identify effected pathways and related genes.
resultsWe found that immune response, cell chemotaxis, inflammation, cytoskeleton organization are significantly deregulated in ischemic zone as early response within 30 min. Unexpectedly, there were several affected signaling pathways such as cell chemotaxis, regulation of endothelial cell proliferation, and regulation of caveolea regulation of anti-apoptosis, regulation of cytoskeleton organization and cell adhesion on the remote zone in the right ventricle.
conclusionThis data demonstrates that there is an immediate molecular response in both ventricles after an AMI. Although the ischemia did not histologically involve the right ventricle; there is a clear molecular response to the infarct in the left ventricle. This provides us new insights to understand molecular mechanisms behind AMI and to find more effective drug targets.
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