ArticleInternational journal of molecular sciences2015
MiR-25 protects cardiomyocytes against oxidative damage by targeting the mitochondrial calcium uniporter.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 citations in OpenAlex.
- Associations of osteopontin and NT-proBNP with circulating miRNA levels in acute coronary syndrome.Physiological genomics · 2019Trial
- Dynamic rewiring of microRNA networks in the brainstem autonomic control circuits during hypertension development in the female spontaneously hypertensive rat.Physiological genomics · 2025Article
- NADPH Oxidases in Cancer Therapy-Induced Cardiotoxicity: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- A Thorough Navigation of miRNA's Blueprint in Crafting Cardiovascular Fate.Health science reports · 2024Article
- Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection.Basic research in cardiology · 2024Review
- Extracellular Vesicles in Diabetic Cardiomyopathy-State of the Art and Future Perspectives.International journal of molecular sciences · 2024Review
- The phosphokinase activity of IRE1ɑ prevents the oxidative stress injury through miR-25/Nox4 pathway after ICH.CNS neuroscience & therapeutics · 2024Article
- Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.Biomolecules · 2023Review
- Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Role of c-Src and reactive oxygen species in cardiovascular diseases.Molecular genetics and genomics : MGG · 2023Review
- Transcriptome Profiling of the Liver in Nellore Cattle Phenotypically Divergent for RFI in Two Genetic Groups.Animals : an open access journal from MDPI · 2023Article
- Extracellular Vesicle Content Changes Induced by Melatonin Promote Functional Recovery of Pancreatic Beta Cells in Acute Pancreatitis.Journal of inflammation research · 2023Article
- CircHSPG2 absence weakens hypoxia-induced dysfunction in cardiomyocytes by targeting the miR-25-3p/PAWR axis.Cardiovascular diagnosis and therapy · 2022Article
- Mitochondrial calcium exchange in physiology and disease.Physiological reviews · 2022Review
- MiR-25 overexpression inhibits titanium particle-induced osteoclast differentiation via down-regulation of mitochondrial calcium uniporter in vitro.Journal of orthopaedic surgery and research · 2022Article
- Role of MicroRNAs in Extreme Animal Survival Strategies.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Review
- Non-coding RNAs in cardiac regeneration: Mechanism of action and therapeutic potential.Seminars in cell & developmental biology · 2021Review
- A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration.Nature communications · 2021Article
- Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been documented to be abundant in cardiomyocytes, but its function in the heart remains unknown. Here, we report that miR-25 can protect cardiomyocytes against oxidative damage by down-regulating mitochondrial calcium uniporter (MCU). MiR-25 was markedly elevated in response to oxidative stimulation in cardiomyocytes. Further overexpression of miR-25 protected cardiomyocytes against oxidative damage by inactivating the mitochondrial apoptosis pathway. MCU was identified as a potential target of miR-25 by bioinformatical analysis. MCU mRNA level was reversely correlated with miR-25 under the exposure of H2O2, and MCU protein level was largely decreased by miR-25 overexpression. The luciferase reporter assay confirmed that miR-25 bound directly to the 3' untranslated region (UTR) of MCU mRNA. MiR-25 significantly decreased H2O2-induced elevation of mitochondrial Ca2+ concentration, which is likely to be the result of decreased activity of MCU. We conclude that miR-25 targets MCU to protect cardiomyocytes against oxidative damages. This finding provides novel insights into the involvement of miRNAs in oxidative stress in cardiomyocytes.
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