ArticleDisease models & mechanisms2015
miR-146a targets Fos expression in human cardiac cells.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Matrix Dynamics and Microbiome Crosstalk: Matrix Metalloproteinases as Key Players in Disease and Therapy.International journal of molecular sciences · 2025Review
- Evaluation of miR-146a as a potential biomarker for diagnosis of cardiotoxicity induced by chemotherapy in patients with breast cancer.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025Article
- The Potential of Mesenchymal Stem Cell-Derived Exosomes in Cardiac Repair.International journal of molecular sciences · 2024Review
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Unraveling Therapeutic Opportunities and the Diagnostic Potential of microRNAs for Human Lung Cancer.Pharmaceutics · 2023Review
- Cardiac Biomarkers and Their Role in Identifying Increased Risk of Cardiovascular Complications in COVID-19 Patients.Diagnostics (Basel, Switzerland) · 2023Review
- NONHSAT098487.2 protects cardiomyocytes from oxidative stress injury by regulating the Notch pathway.Heliyon · 2023Article
- Alterations in Circulating miRNA Levels after Infection with SARS-CoV-2 Could Contribute to the Development of Cardiovascular Diseases: What We Know So Far.International journal of molecular sciences · 2023Review
- Identification of diagnostic immune-related gene biomarkers for predicting heart failure after acute myocardial infarction.Open medicine (Warsaw, Poland) · 2023Article
- Targeting TLR2/Rac1/cdc42/JNK Pathway to Reveal That Ruxolitinib Promotes Thrombocytopoiesis.International journal of molecular sciences · 2022Article
- MicroRNA-146: Biomarker and Mediator of Cardiovascular Disease.Disease markers · 2022Review
- Network pharmacology and RNA-sequencing reveal the molecular mechanism of Xuebijing injection on COVID-19-induced cardiac dysfunction.Computers in biology and medicine · 2021Article
- MicroRNAs and long non-coding RNAs in the pathophysiological processes of diabetic cardiomyopathy: emerging biomarkers and potential therapeutics.Cardiovascular diabetology · 2021Review
- MiR-146a mediates TLR-4 signaling pathway to affect myocardial fibrosis in rat constrictive pericarditis model.Journal of thoracic disease · 2021Article
- microRNAs involved in psoriasis and cardiovascular diseases.Vascular biology (Bristol, England) · 2021Review
- Extracellular vesicular microRNAs as potential biomarker for early detection of doxorubicin-induced cardiotoxicity.Journal of veterinary internal medicine · 2020Article
- Increased matrix metalloproteinases expression in tuberous sclerosis complex: modulation by microRNA 146a and 147b in vitro.Neuropathology and applied neurobiology · 2020Article
- Transcriptome analysis defines myocardium gene signatures in children with ToF and ASD and reveals disease-specific molecular reprogramming in response to surgery with cardiopulmonary bypass.Journal of translational medicine · 2020Article
- Inhibition of microRNA-146a attenuated heart failure in myocardial infarction rats.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
miR-146a is a microRNA whose transcript levels are induced in the heart upon activation of NF-κB, a transcription factor induced by pro-inflammatory molecules (such as TNF-α) that is strongly related to the pathogenesis of cardiac disorders. The main goal of this study consisted of studying new roles of miR-146a in cardiac pathological processes caused by the pro-inflammatory cytokine TNF-α. Our results demonstrate that miR-146a transcript levels were sharply increased in cardiac ventricular tissue of transgenic mice with specific overexpression of TNF-α in the heart, and also in a cardiomyocyte cell line of human origin (AC16) exposed to TNF-α. Among all the in silico predicted miR-146a target genes, Fos mRNA and protein levels notably decreased after TNF-α treatment or miR-146a overexpression. These changes correlated with a diminution in the DNA-binding activity of AP-1, the Fos-containing transcription factor complex. Interestingly, AP-1 inhibition was accompanied by a reduction in matrix metalloproteinase (MMP)-9 mRNA levels in human cardiac cells. The specific regulation of this MMP by miR-146a was further confirmed at the secretion and enzymatic activity levels, as well as after anti-miR-mediated miR-146a inhibition. The results reported here demonstrate that Fos is a direct target of miR-146a activity and that downregulation of the Fos-AP-1 pathway by miR-146a has the capacity to inhibit MMP-9 activity. Given that MMP-9 is an AP-1 target gene involved in cardiac remodeling, myocardial dysfunction and progression of heart failure, these findings suggest that miR-146a might be a new and promising therapeutic tool for treating cardiac disorders associated with enhanced inflammation in the heart.
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