ArticleMedical hypotheses2013
Ephrin-Eph signaling as a potential therapeutic target for the treatment of myocardial infarction.
Article in Medical hypotheses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Administration of Single or Repeated Doses of CDCs in a Swine Model of Reperfused Myocardial Infarction: Magnetic Resonance and Proteomics Evaluation.International journal of molecular sciences · 2025Article
- Single-cell genomics improves the discovery of risk variants and genes of atrial fibrillation.Nature communications · 2023Article
- Long-term exposure to ambient fine particulate components and leukocyte epigenome-wide DNA Methylation in older men: the Normative Aging Study.Environmental health : a global access science source · 2023Article
- MicroRNA profiling of the feline left heart identifies chamber-specific expression signatures in health and in advanced hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2023Article
- Multiomic analyses reveal enriched glycolytic processes in β-myosin heavy chain-expressed cardiomyocytes in early cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2022Article
- Signaling Pathways Involved in Myocardial Ischemia-Reperfusion Injury and Cardioprotection: A Systematic Review of Transcriptomic Studies inJournal of cardiovascular development and disease · 2022Review
- A Concise Review on Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Personalized Regenerative Medicine.Stem cell reviews and reports · 2021Review
- Identification of tetracycline combinations as EphB1 tyrosine kinase inhibitors for treatment of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- EphrinA1-Fc Attenuates Ventricular Remodeling and Dysfunction in Chronically Nonreperfused WT but not EphA2-R-M mice.International journal of molecular sciences · 2020Article
- Intracardiac administration of ephrinA1-Fc preserves mitochondrial bioenergetics during acute ischemia/reperfusion injury.Life sciences · 2019Article
- Use of Multifactorial Treatments to Address the Challenge of Translating Experimental Myocardial Infarct Reduction Strategies.International journal of molecular sciences · 2019Review
- The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells.BMC genomics · 2018Article
- Anatomical-Molecular Distribution of EphrinA1 in Infarcted Mouse Heart Using MALDI Mass Spectrometry Imaging.Journal of the American Society for Mass Spectrometry · 2018Article
- Article
- EphA2-receptor deficiency exacerbates myocardial infarction and reduces survival in hyperglycemic mice.Cardiovascular diabetology · 2014Article
- Deletion of the EphA2 receptor exacerbates myocardial injury and the progression of ischemic cardiomyopathy.Frontiers in physiology · 2014Article
- Circadian rhythms, Wnt/beta-catenin pathway and PPAR alpha/gamma profiles in diseases with primary or secondary cardiac dysfunction.Frontiers in physiology · 2014Review
- Evidence-based treatment strategies for hypoplastic left heart syndrome: The role of EFNA1/EphA.Annals of pediatric cardiologyReview
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Although numerous strategies have been developed to reduce the initial ischemic insult and cellular injury that occurs during myocardial infarction (MI), few have progressed into the clinical arena. The epidemiologic and economic impact of MI necessitates the development of innovative therapies to rapidly and effectively reduce the initial injury and subsequent cardiac dysfunction. The Eph receptors and their cognate ligands, the ephrins, are the largest family of receptor tyrosine kinases, and their signaling has been shown to play a diverse role in various cellular processes. The recent advances in the study of ephrin-Eph signaling have shown promising progress in many fields of medicine. They have been implicated in the pathophysiology of various cancers and in the regulation of inflammation and apoptosis. Recent studies have shown that manipulation of ephrin-Eph cell signaling can favorably influence cardiomyocyte viability and ultimately preserve cardiac function post-MI. In this article, we explore the hypothesis that manipulation of ephrin-Eph signaling may potentially be a novel therapeutic target in the treatment of MI through alteration of the cellular processes that govern injury and wound healing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.