ArticleJCI insight2018
Inhibition of profibrotic microRNA-21 affects platelets and their releasate.
Article in JCI insight, 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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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
18 citing papers in PubMed, 40 citations in OpenAlex.
- Platelets and inflammation-insights from platelet non-coding RNA content and release in the Bruneck study and the PACMAN-AMI trial.Cardiovascular research · 2025Trial
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- Platelet-enriched microRNAs as novel biomarkers in atherosclerotic and cardiovascular disease patients.ARYA atherosclerosis · 2024Review
- Platelet microRNAs as Potential Novel Biomarkers for Antiplatelet Therapy with P2YJournal of clinical medicine · 2023Article
- Platelets and the Atherosclerotic Process: An Overview of New Markers of Platelet Activation and Reactivity, and Their Implications in Primary and Secondary Prevention.Journal of clinical medicine · 2023Review
- Challenges and promise of targeting miRNA in rheumatic diseases: a computational approach to identify miRNA association with cell types, cytokines, and disease mechanisms.Frontiers in immunology · 2023Review
- Sex-specific analysis of microRNA profiles in HBV-associated cirrhosis by small RNA-sequencing.Hepatology communications · 2022Article
- The downregulation of miR-22 and miR-372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway.Journal of clinical laboratory analysis · 2022Article
- Insights Into Platelet-Derived MicroRNAs in Cardiovascular and Oncologic Diseases: Potential Predictor and Therapeutic Target.Frontiers in cardiovascular medicine · 2022Review
- Context-Dependent miR-21 Regulation of TLR7-Mediated Autoimmune and Foreign Antigen-Driven Antibody-Forming Cell and Germinal Center Responses.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Methods to Investigate miRNA Function: Focus on Platelet Reactivity.Thrombosis and haemostasis · 2021Review
- Metabolic recovery after weight loss surgery is reflected in serum microRNAs.BMJ open diabetes research & care · 2020Article
- microRNAs as promising biomarkers of platelet activity in antiplatelet therapy monitoring.International journal of molecular sciences · 2020Review
- Circulating MicroRNA Levels Indicate Platelet and Leukocyte Activation in Endotoxemia Despite Platelet P2YInternational journal of molecular sciences · 2020Article
- miR-21-KO Alleviates Alveolar Structural Remodeling and Inflammatory Signaling in Acute Lung Injury.International journal of molecular sciences · 2020Article
- Thrombin, a Mediator of Coagulation, Inflammation, and Neurotoxicity at the Neurovascular Interface: Implications for Alzheimer's Disease.Frontiers in neuroscience · 2020Review
- Small extracellular vesicles deliver miR-21 and miR-217 as pro-senescence effectors to endothelial cells.Journal of extracellular vesicles · 2020Article
- Antisense Oligonucleotide Inhibition of MicroRNA-494 Halts Atherosclerotic Plaque Progression and Promotes Plaque Stabilization.Molecular therapy. Nucleic acids · 2019Article
Corrections and comments
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Authors and funding
30 authors at 9 institutions in 5 countries.
Funding
Abstract
Fibrosis is a major contributor to organ disease for which no specific therapy is available. MicroRNA-21 (miR-21) has been implicated in the fibrogenetic response, and inhibitors of miR-21 are currently undergoing clinical trials. Here, we explore how miR-21 inhibition may attenuate fibrosis using a proteomics approach. Transfection of miR-21 mimic or inhibitor in murine cardiac fibroblasts revealed limited effects on extracellular matrix (ECM) protein secretion. Similarly, miR-21-null mouse hearts showed an unaltered ECM composition. Thus, we searched for additional explanations as to how miR-21 might regulate fibrosis. In plasma samples from the community-based Bruneck Study, we found a marked correlation of miR-21 levels with several platelet-derived profibrotic factors, including TGF-β1. Pharmacological miR-21 inhibition with an antagomiR reduced the platelet release of TGF-β1 in mice. Mechanistically, Wiskott-Aldrich syndrome protein, a negative regulator of platelet TGF-β1 secretion, was identified as a direct target of miR-21. miR-21-null mice had lower platelet and leukocyte counts compared with littermate controls but higher megakaryocyte numbers in the bone marrow. Thus, to our knowledge this study reports a previously unrecognized effect of miR-21 inhibition on platelets. The effect of antagomiR-21 treatment on platelet TGF-β1 release, in particular, may contribute to the antifibrotic effects of miR-21 inhibitors.
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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.