ArticleOncotarget2017
Analysis of region specific gene expression patterns in the heart and systemic responses after experimental myocardial ischemia.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction.Rejuvenation research · 2025Review
- NKX2-5 regulates vessel remodeling in scleroderma-associated pulmonary arterial hypertension.JCI insight · 2024Article
- Ribonucleicacid interference or small molecule inhibition of Runx1 in the border zone prevents cardiac contractile dysfunction following myocardial infarction.Cardiovascular research · 2023Article
- Interaction between Acute Hepatic Injury and Early Coagulation Dysfunction on Mortality in Patients with Acute Myocardial Infarction.Journal of clinical medicine · 2023Article
- Spatiotemporal transcriptome analysis reveals critical roles for mechano-sensing genes at the border zone in remodeling after myocardial infarction.Nature cardiovascular research · 2022Article
- GSK3β Inhibition Is the Molecular Pivot That Underlies the Mir-210-Induced Attenuation of Intrinsic Apoptosis Cascade during Hypoxia.International journal of molecular sciences · 2022Article
- Signaling Pathways Involved in Myocardial Ischemia-Reperfusion Injury and Cardioprotection: A Systematic Review of Transcriptomic Studies inJournal of cardiovascular development and disease · 2022Review
- Article
- Epigenetic State Changes Underlie Metabolic Switch in Mouse Post-Infarction Border Zone Cardiomyocytes.Journal of cardiovascular development and disease · 2021Article
- Working together.eLife · 2021Article
- Unraveling the Metabolic Derangements Occurring in Non-infarcted Areas of Pig Hearts With Chronic Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- PACAP neuropeptide promotes Hepatocellular Protection via CREB-KLF4 dependent autophagy in mouse liver Ischemia Reperfusion Injury.Theranostics · 2020Article
- The Arginase Pathway in Neonatal Brain Hypoxia-Ischemia.Developmental neuroscience · 2018Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsIschemic myocardial injury leads to the activation of inflammatory mechanisms and results in ventricular remodeling. Although great efforts have been made to unravel the molecular and cellular processes taking place in the ischemic myocardium, little is known about the effects on the surrounding tissue and other organs. The aim of this study was to determine region specific differences in the myocardium and in distant organs after experimental myocardial infarction by using a bioinformatics approach. METHODS AND
resultsA porcine closed chest reperfused acute myocardial infarction model and mRNA microarrays have been used to evaluate gene expression changes. Myocardial infarction changed the expression of 8903 genes in myocardial-, 856 in hepatic- and 338 in splenic tissue. Identification of myocardial region specific differences as well as expression profiling of distant organs revealed clear gene-regulation patterns within the first 24 hours after ischemia. Transcription factor binding site analysis suggested a strong role for Kruppel like factor 4 (Klf4) in the regulation of gene expression following myocardial infarction, and was therefore investigated further by immunohistochemistry. Strong nuclear Klf4 expression with clear region specific differences was detectable in porcine and human heart samples after myocardial infarction.
conclusionApart from presenting a post myocardial infarction gene expression database and specific response pathways, the key message of this work is that myocardial ischemia does not end at the injured myocardium. The present results have enlarged the spectrum of organs affected, and suggest that a variety of organ systems are involved in the co-ordination of the organism´s response to myocardial infarction.
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