ArticleAmerican journal of translational research2020
The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Emerging Epigenetic Therapies for the Treatment of Cardiac Fibrosis.Biomedicines · 2025Review
- Nanog overexpression enhances the therapeutic efficacy of ADMSCs in AMI rats via the upregulation of JAK/STAT3 signaling and cyclin-mitochondrial expression.International journal of biological sciences · 2025Article
- Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data.Current pharmaceutical design · 2024Review
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Safety and efficacy of intracoronary artery administration of human bone marrow-derived mesenchymal stem cells in STEMI of Lee-Sung pigs-A preclinical study for supporting the feasibility of the OmniMSC-AMI phase I clinical trial.Frontiers in cardiovascular medicine · 2023Article
- Synergic Effect of Early Administration of Probiotics and Adipose-Derived Mesenchymal Stem Cells on Alleviating Inflammation-Induced Chronic Neuropathic Pain in Rodents.International journal of molecular sciences · 2022Article
- Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction.Biomedicines · 2022Review
- H3K9me2 regulation of BDNF expression via G9a partakes in the progression of heart failure.BMC cardiovascular disorders · 2022Article
- Epigenetic regulation in myocardial infarction: Non-coding RNAs and exosomal non-coding RNAs.Frontiers in cardiovascular medicine · 2022Review
- Inhibition of histone methyltransferase G9a effectively protected the kidney against ischemia-reperfusion injury.American journal of translational research · 2022Article
- CHD4 as an important mediator in regulating the malignant behaviors of colorectal cancer.International journal of biological sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study tested the hypothesis that combined histone methyltransferase G9a inhibitor (i.e., UNC0638) and erythropoietin (EPO) was superior to either one alone for protecting myocardium from acute myocardial infarction (AMI) damage. METHODS AND
resultsAdult-male SD rats (n=30) were equally categorized into group 1 (sham-operated control), group 2 (AMI), group 3 (AMI-EPO/1000 IU/kg, I.M./3 h after AMI), group 4 (AMI- UNC0638/5 mg/kg I.P./3 h after AMI) and group 5 [AMI-UNC0638-EPO 3 h after AMI] treatment. Animals were euthanized at day 21 after AMI induction. By day 21, left-ventricular-ejection-fraction (LVEF) was highest in group 1, lowest in group 2, significantly higher in group 5 than in groups 3 and 4, but no difference between the latter two groups (all P<0.0001). The protein expressions of inflammatory (MMP-2/MM-9), fibrotic (fibronectin/Smad3/TGF-ß), apoptotic/DNA-damaged (caspas-3/PARP/γ-H2AX), cell-stress response (HIF-1α/p-Akt/p-mTOR) and autophagic (beclin-1/ratio of LC3B-II to LC3B-I) biomarkers exhibited an opposite pattern, whereas the protein expressions of endothelial integrity (CD31/vWF) and anti-oxidant (SIRT1/SIRT3) exhibited an identical pattern of LVEF among the five groups (all P<0.0001). The protein expressions (SDF-1α/VEGF/CXCR4) and cellular expressions (C-kit/CD31+//Sca-1/CD31+//KDR/CD34+) of angiogenesis biomarkers were significantly progressively increased from groups 1 to 5 (all P<0.0001). The infarction/fibrotic areas, myocyte size and number of G9a cells exhibited an opposite pattern, whereas the small-vessel density displayed an identical trend of LVEF among the groups (all P<0.0001). Flow cytometric analysis showed cellular levels of inflammation (Ly6G+/MPO+/CD11b/c+), oxidative-stress (DCFDA+) and apoptosis (early+/late+) exhibited an opposite pattern to LVEF among the groups (all P<0.0001).
conclusionEPO-BIX01294 effectively protected myocardium against AMI-induced damage.
Indexed as
Identifiers
32774698PMC7407701W3049402520What Socratic holds
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 Socratic graph.