ArticleCell stress & chaperones2015
MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network.
Article in Cell stress & chaperones, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Circulating microRNA-1 as a diagnostic biomarker for acute myocardial infarction: a meta-analysis.Cardiology journal · 2025Pooled it
- RNA Therapeutics in Heart Failure.Journal of cardiovascular translational research · 2025Review
- The emerging role of Nrf2 in heart failure: From cardioprotection to therapeutic approaches.ESC heart failure · 2025Review
- Identification of Connexin 26 on Extracellular Vesicles from Human Cardiomyocytes and Plasma: Novel Insights into miRNA Loading and Oxidative Injury.International journal of molecular sciences · 2025Article
- Emerging Circulating Biomarkers for Enhanced Cardiovascular Risk Prediction.Journal of lipid and atherosclerosis · 2024Review
- Cardiovascular Disease and miRNAs: Possible Oxidative Stress-Regulating Roles of miRNAs.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- In silico based analysis to explore genetic linkage between atherosclerosis and its potential risk factors.Biochemistry and biophysics reports · 2023Article
- Multiple Copies of microRNA Binding Sites in Long 3'UTR Variants Regulate Axonal Translation.Cells · 2023Article
- The active ingredient (DSH-20) of Salvia miltiorrhiza flower reduces oxidative damage and apoptosis in cardiomyocytes by regulating miR-1.Molecular biology reports · 2022Article
- MicroRNAs as Potential Biomarkers in Pituitary Adenomas.Non-coding RNA · 2021Review
- Evaluation of Oxidative Stress, Apoptosis, and Expression of MicroRNA-208a and MicroRNA-1 in Cardiovascular Patients.Reports of biochemistry & molecular biology · 2021Article
- Regulation of Nrf2 signaling pathway in heart failure: Role of extracellular vesicles and non-coding RNAs.Free radical biology & medicine · 2021Review
- Protective impact ofToxicology research · 2021Article
- Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes.Stem cell research & therapy · 2021Review
- MicroRNA-Related Strategies to Improve Cardiac Function in Heart Failure.Frontiers in cardiovascular medicine · 2021Review
- The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020Review
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Oxidative Stress-Responsive MicroRNAs in Heart Injury.International journal of molecular sciences · 2020Review
- MiR-1/133 attenuates cardiomyocyte apoptosis and electrical remodeling in mice with viral myocarditis.Cardiology journal · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress plays an important role in cardiovascular diseases. Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alterations in the expression of proteins related to oxidative stress, which could contribute to heart dysfunction. We compared cardiac function in wild-type (WT) and miR-1 transgene (miR-1/Tg) C57BL/6 mice (n ≥ 10/group). Echocardiography showed that stroke volume (SV), ejection fraction (EF), and fractional shortening (FS) were significantly decreased in miR-1/Tg mice. Concomitantly, the level of reactive oxygen species (ROS) was elevated in the cardiomyocytes from the miR-1/Tg mice, and activities of lactate dehydrogenase (LDH) and creatinine kinase (CK) in plasma were also increased in the miR-1/Tg mice. All of these changes could be reversed by LNA-anti-miR-1. In the cardiomyocytes of neonatal Wistar rats, overexpression of miR-1 exhibits higher ROS levels and lower resistance to H2O2-induced oxidative stress. We demonstrated that SOD1, Gclc, and G6PD are novel targets of miR-1 for post-transcriptional repression. MicroRNA-1 post-transcriptionally represses the expression of SOD1, Gclc, and G6PD, which is likely to contribute to the increased ROS level and the susceptibility to oxidative stress of the hearts of miR-1 transgenic mice.
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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.