ArticleThe American journal of pathology2003
NCAM(CD56) and RUNX1(AML1) are up-regulated in human ischemic cardiomyopathy and a rat model of chronic cardiac ischemia.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Integrative functional analysis of super enhancer SNPs for coronary artery disease.Journal of human genetics · 2018Pooled it
- Identification of RUNX1 as a Biomarker for Right Ventricular Remodeling in Pulmonary Arterial Hypertension Using WGCNA.Pulmonary circulation · 2026Article
- A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure.Nature cardiovascular research · 2026Article
- A novel cardiomyopathy phenotype linked to a CHD7 missense variant.Scientific reports · 2025Article
- NCAM1 modulates the proliferation and migration of pulmonary arterial smooth muscle cells in pulmonary hypertension.Respiratory research · 2024Article
- The Current State of Realistic Heart Models for Disease Modelling and Cardiotoxicity.International journal of molecular sciences · 2024Review
- Pharmacological inhibition of RUNX1 reduces infarct size after acute myocardial infarction in rats and underlying mechanism revealed by proteomics implicates repressed cathepsin levels.Functional & integrative genomics · 2024Article
- Asparagine Synthetase Marks a Distinct Dependency Threshold for Cardiomyocyte Dedifferentiation.Circulation · 2024Article
- Ribonucleicacid interference or small molecule inhibition of Runx1 in the border zone prevents cardiac contractile dysfunction following myocardial infarction.Cardiovascular research · 2023Article
- Age-related promoter-switch regulates Runx1 expression in adult rat hearts.BMC cardiovascular disorders · 2023Article
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Genetics and Molecular Basis of Congenital Heart Defects in Down Syndrome: Role of Extracellular Matrix Regulation.International journal of molecular sciences · 2023Review
- MiR-199a-3p Restrains Foaming and Inflammation by Regulating RUNX1 in Macrophages.Molecular biotechnology · 2022Article
- Article
- Relationship betweenJournal of thoracic disease · 2021Article
- Runt-related transcription factor 1 (Runx1) aggravates pathological cardiac hypertrophy by promoting p53 expression.Journal of cellular and molecular medicine · 2021Article
- Zebrafish cardiac regeneration-looking beyond cardiomyocytes to a complex microenvironment.Histochemistry and cell biology · 2020Review
- RUNX1: an emerging therapeutic target for cardiovascular disease.Cardiovascular research · 2020Review
- Runx1 promotes scar deposition and inhibits myocardial proliferation and survival during zebrafish heart regeneration.Development (Cambridge, England) · 2020Article
- Hematopoietic Stem Cell Transcription Factors in Cardiovascular Pathology.Frontiers in genetics · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myocardial ischemia is the leading cause of impaired myocardial contractility and heart failure. To identify differentially expressed genes in human ischemic cardiomyopathy (ICM), we constructed a subtracted cDNA library using specimens of ICM compared to normal human heart. Among 100 randomly sequenced clones, seven sequences represented recently identified candidate genes for differential expression in cardiac hypertrophy. A further clone without a known hypertrophy-association coded for the adhesion molecule NCAM(CD56). RNase protection assay, immunohistochemistry, and Western blotting revealed strong overexpression of NCAM(CD56) in all hearts with ICM (n = 14) compared to normal hearts (n = 8), whereas in congestive cardiomyopathy (CCM) (n = 8), hypertrophic obstructive cardiomyopathy (n = 2), myocarditis (n = 4), and sarcoidosis (n = 2), at most slight overexpression of NCAM(CD56) was observed. NCAM(CD56) overexpression abnormally involved the whole cell membrane and the cytoplasma of cardiomyocytes only inside and adjacent to ischemia-induced cardiac scars. Normal or hypertrophic fibers at a distance from ischemic scars were devoid of NCAM overexpression. Identical alterations were observed in an experimental rat ICM model, but not in normal nor in spontaneously hypertensive rat hearts. In search of NCAM(CD56)-related transcription factors we found RUNX1(AML1) up-regulation in ICM and detected RUNX1(AML1) binding within the NCAM(CD56) promoter by electromobility shift assay. We concluded that strong overexpression of NCAM(CD56) and RUNX1(AML1) is a constant and characteristic feature of cardiomyocytes within or adjacent to scars in ICM.
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