ArticleJournal of the American Heart Association2019
MicroRNA-101 Protects Against Cardiac Remodeling Following Myocardial Infarction via Downregulation of Runt-Related Transcription Factor 1.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved ejection fraction.Cardiovascular research · 2026Article
- CPSF6-mediated alternative polyadenylation of RUNX1 to regulate silica-induced pulmonary fibrosis progression.Respiratory research · 2026Article
- Distinct circular RNA signatures distinguish STEMI from NSTEMI in acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Runx1 drives cardiac fibrosis and heart failure through epigenetic activation of myofibroblasts in pressure overload-induced cardiac remodeling.BMC cardiovascular disorders · 2025Article
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Investigating the expression level of miR-17-3p, miR-101-3p, miR-335-3p, and miR-296-3p in the peripheral blood of patients with acute myocardial infarction.Molecular and cellular biochemistry · 2024Article
- Brg1 and RUNX1 synergy in regulating TRPM4 channel in mouse cardiomyocytes.Frontiers in pharmacology · 2024Article
- Identification of genetic associations between acute myocardial infarction and non-small cell lung cancer.Frontiers in molecular biosciences · 2024Article
- Ribonucleicacid interference or small molecule inhibition of Runx1 in the border zone prevents cardiac contractile dysfunction following myocardial infarction.Cardiovascular research · 2023Article
- Clinical Variables Influence the Ability of miR-101, miR-150, and miR-21 to Predict Ventricular Remodeling after ST-Elevation Myocardial Infarction.Biomedicines · 2023Article
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- Noncoding RNAs and Cardiac Fibrosis.Reviews in cardiovascular medicine · 2023Review
- Signs and signals limiting myocardial damage using PICSO: a scoping review decoding paradigm shifts toward a new encounter.Frontiers in cardiovascular medicine · 2023Article
- Targeting RUNX1 as a novel treatment modality for pulmonary arterial hypertension.Cardiovascular research · 2022Article
- Natural emodin reduces myocardial ischemia/reperfusion injury by modulating the RUNX1/miR‑142‑3p/DRD2 pathway and attenuating inflammation.Experimental and therapeutic medicine · 2022Article
- β-Catenin promotes long-term survival and angiogenesis of peripheral blood mesenchymal stem cells via the Oct4 signaling pathway.Experimental & molecular medicine · 2022Article
- The circRNA-miRNA/RBP regulatory network in myocardial infarction.Frontiers in pharmacology · 2022Review
- Diagnostic utility of circulating plasma microRNA-101a in severity of coronary heart disease.Irish journal of medical science · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Myocardial infarction (MI) generally leads to heart failure and sudden death. The hearts of people with MI undergo remodeling with the features of expanded myocardial infarct size and dilated left ventricle. Many microRNAs (miRs) have been revealed to be involved in the remodeling process; however, the participation of miR-101 remains unknown. Therefore, this study aims to find out the regulatory mechanism of miR-101 in MI-induced cardiac remodeling. Methods and Results Microarray data analysis was conducted to screen differentially expressed genes in MI. The rat model of MI was established by left coronary artery ligation. In addition, the relationship between miR-101 and runt-related transcription factor 1 (RUNX1) was identified using dual luciferase reporter assay. After that, the rats injected with lentiviral vector expressing miR-101 mimic, inhibitor, or small interfering RNA against RUNX1 were used to examine the effects of miR-101 and RUNX1 on transforming growth factor β signaling pathway, cardiac function, infarct size, myocardial fibrosis, and cardiomyocyte apoptosis. RUNX1 was highly expressed, while miR-101 was poorly expressed in MI. miR-101 was identified to target RUNX1. Following that, it was found that overexpression of miR-101 or silencing of RUNX1 improved the cardiac function and elevated left ventricular end-diastolic and end-systolic diameters. Also, miR-101 elevation or RUNX1 depletion decreased infarct size, myocardial fibrosis, and cardiomyocyte apoptosis. Moreover, miR-101 could negatively regulate RUNX1 to inactivate the transforming growth factor β1/Smad family member 2 signaling pathway. Conclusions Taken together, miR-101 plays a protective role against cardiac remodeling following MI via inactivation of the RUNX1-dependent transforming growth factor β1/Smad family member 2 signaling pathway, proposing miR-101 and RUNX1 as potential therapeutic targets for 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.