ArticleJournal of molecular and cellular cardiology2016
S100A4 protects the myocardium against ischemic stress.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- S100A4 expression in the enteric nerve system of young and aged rats.Molecular biology reports · 2026Article
- Extracorporeal cardiac shock wave therapy modulates post-infarction neovascularization via CAC-mediated pro-angiogenic effects and modulation of the S100A4/CSF2/FOXO1 protein network.Frontiers in cardiovascular medicine · 2026Article
- S100A4-shRNA mitigates autophagy, reduces inflammation, and improves cardiac functionality in MIRI.International journal of cardiology. Cardiovascular risk and prevention · 2025Article
- S100A1ct: A Synthetic Peptide Derived From S100A1 Protein Improves Cardiac Performance and Survival in Preclinical Heart Failure Models.Circulation · 2025Article
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- S100A4 Is a Key Facilitator of Thoracic Aortic Dissection.International journal of biological sciences · 2024Article
- Immune-related biomarkers in myocardial infarction; diagnostic/prognostic value and therapeutic potential.Journal of biochemical and molecular toxicology · 2023Review
- An Update on MYBPC3 Gene Mutation in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023Review
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Role of Heme-Oxygenase-1 in Biology of Cardiomyocytes Derived from Human Induced Pluripotent Stem Cells.Cells · 2021Article
- S100A4 in Spinal Substantia Gelatinosa from Dorsal Root Ganglia Modulates Neuropathic Pain in a Rodent Spinal Nerve Injury Model.Journal of pain research · 2021Article
- Modulation of SERCA2a expression and function by ultrasound-guided myocardial gene transfection.Experimental and therapeutic medicine · 2020Article
- MiR-489 aggravates H2O2-induced apoptosis of cardiomyocytes via inhibiting IGF1.Bioscience reports · 2020Article
- Diagnostic and Prognostic Biomarkers for Myocardial Infarction.Frontiers in cardiovascular medicine · 2020Review
- A Multi-Network Comparative Analysis of Transcriptome and Translatome Identifies Novel Hub Genes in Cardiac Remodeling.Frontiers in genetics · 2020Article
- FSP1 promotes the biofunctions of adventitial fibroblast through the crosstalk among RAGE, JAK2/STAT3 and Wnt3a/β-catenin signalling pathways.Journal of cellular and molecular medicine · 2019Article
- RhoA regulates Drp1 mediated mitochondrial fission through ROCK to protect cardiomyocytes.Cellular signalling · 2018Article
- S100A4 as a Target of the E3-Ligase Asb2β and Its Effect on Engineered Heart Tissue.Frontiers in physiology · 2018Article
- Evaluation of MYBPC3 trans-Splicing and Gene Replacement as Therapeutic Options in Human iPSC-Derived Cardiomyocytes.Molecular therapy. Nucleic acids · 2017Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundMyocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue fibrosis. S100A4 protein plays multiple roles in cellular survival, and tissue fibrosis, but the relative role of the S100A4 in the myocardium after myocardial infarction is unknown. This study aims to investigate the role of S100A4 in myocardial remodeling and cardiac function following infarct damage. METHODS AND
resultsS100A4 expression is low in the adult myocardium, but significantly increased following myocardial infarction. Deletion of S100A4 increased cardiac damage after myocardial infarction, whereas cardiac myocyte-specific overexpression of S100A4 protected the infarcted myocardium. Decreased cardiac function in S100A4 Knockout mice was accompanied with increased cardiac remodeling, fibrosis, and diminished capillary density in the remote myocardium. Loss of S100A4 caused increased apoptotic cell death both in vitro and in vivo in part mediated by decreased VEGF expression. Conversely, S100A4 overexpression protected cells against apoptosis in vitro and in vivo. Increased pro-survival AKT-signaling explained reduced apoptosis in S100A4 overexpressing cells.
conclusionS100A4 expression protects cardiac myocytes against myocardial ischemia and is required for stabilization of cardiac function after MI.
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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.