ArticleScientific reports2018
A novel system-level approach using RNA-sequencing data identifies miR-30-5p and miR-142a-5p as key regulators of apoptosis in myocardial infarction.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- ATAD3B and SKIL polymorphisms associated with antipsychotic-induced QTc interval change in patients with schizophrenia: a genome-wide association study.Translational psychiatry · 2022Trial
- RNA Sequencing and Targeted Knockdown Reveal miR-142a-5p as a Driver of Retinal Degeneration in rd1 Mice.Biology · 2026Article
- Post-infarction KLHL40-mediated regulation of cardiac sarcomeric integrity and function.PeerJ · 2026Article
- Evaluation of Dexmedetomidine-Associated Bradycardia and Related Drug-Drug Interactions Using Electronic Health Record (EHR) and miRNA Target Analysis.Current issues in molecular biology · 2025Article
- MiR- 142 - 3p Up-regulation Mitigates Cerebral Ischemia-reperfusion Injury by Targeting PICALM.Journal of molecular neuroscience : MN · 2025Article
- Matricellular protein CCN1 promotes collagen alignment and scar integrity after myocardial infarction.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
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- Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction.Scientific reports · 2023Article
- Dynamic regulation of HIF-1 signaling in the rhesus monkey heart after ischemic injury.BMC cardiovascular disorders · 2022Article
- Circulating MiR-30b-5p is upregulated in Cavalier King Charles Spaniels affected by early myxomatous mitral valve disease.PloS one · 2022Article
- MicroRNAs-The Heart of Post-Myocardial Infarction Remodeling.Diagnostics (Basel, Switzerland) · 2021Review
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- Cardioprotection of cortistatin against isoproterenol-induced myocardial injury in rats.Annals of translational medicine · 2020Article
- Metabolomic Analysis of the Ameliorative Effect of Enhanced Proline Metabolism on Hypoxia-Induced Injury in Cardiomyocytes.Oxidative medicine and cellular longevity · 2020Article
- Comprehensive circRNA Expression Profile and Construction of circRNAs-Related ceRNA Network in a Mouse Model of Autism.Frontiers in genetics · 2020Article
- Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes.Cell death & disease · 2019Article
- The microRNA in ventricular remodeling: the miR-30 family.Bioscience reports · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study identified microRNAs involved in myocardial infarction (MI) through a novel system-level approach using RNA sequencing data in an MI mouse model. This approach involved the extraction of DEGs and DEmiRs from RNA-seq data in sham and MI samples and the subsequent selection of two miRNAs: miR-30-5p (family) and miR-142a-5p, which were downregulated and upregulated in MI, respectively. Gene Set Enrichment Analysis (GSEA) using the predicted targets of the two miRNAs suggested that apoptosis is an essential gene ontology (GO)-associated term. In vitro functional assays using neonatal rat ventricular myocytes (NRVMs) demonstrated that miR-30-5p is anti-apoptotic and miR-142a-5p is pro-apoptotic. Luciferase assays showed that the apoptotic genes, Picalm and Skil, and the anti-apoptotic genes, Ghr and Kitl, are direct targets of miR-30-5p and miR-142a-5p, respectively. siRNA studies verified the results of the luciferase assays for target validation. The results of the system-level high throughput approach identified a pair of functionally antagonistic miRNAs and their targets in MI. This study provides an in-depth analysis of the role of miRNAs in the pathogenesis of MI which could lead to the development of therapeutic tools. The system-level approach could be used to identify miRNAs involved in variety of other diseases.
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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.