ArticleJournal of extracellular biology2024
Bone marrow-fibroblast progenitor cell-derived small extracellular vesicles promote cardiac fibrosis via miR-21-5p and integrin subunit αV signalling.
Article in Journal of extracellular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- An Overview of How Epigenetics, MicroRNA-21, and Endocrine Disrupting Compounds Affect Oocyte Maturation and Pre-Implantation Embryo Development.Journal of developmental biology · 2026Review
- Beyond Extracellular Vesicle (EV) Hype: Practical Solutions and Remaining Hurdles in EV Research, Manufacturing, and Clinical Translation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Extracellular Vesicle-Based Strategies for the Prevention of Chemotherapy-Induced Cardiotoxicity.Therapeutics and clinical risk management · 2026Review
- Cardiac Circular RNAs CDR1as, Circ-RCAN2, Circ-C12orf29 Show Cell-Specific Hypoxia-Induced Dysregulation and Distinct In Vitro Effects.International journal of molecular sciences · 2025Article
- The role of exosomes in immunopathology and potential therapeutic implications.Cellular & molecular immunology · 2025Review
- Exosome‑mediated crosstalk between the cardiovascular and musculoskeletal systems: Mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Exploring the landscape of exosomes in heart failure: a bibliometric analysis.International journal of surgery (London, England) · 2025Review
- The association of serum hsa-miR-21-5p expression with the severity and prognosis of heart failure with reduced ejection fraction.BMC cardiovascular disorders · 2025Article
- MiR-21-3p inhibitor exerts myocardial protective effects by altering macrophage polarization state and reducing excessive mitophagy.Communications biology · 2024Article
- Extracellular Vesicle-Derived Non-Coding RNAs: Key Mediators in Remodelling Heart Failure.Current issues in molecular biology · 2024Review
Corrections and comments
- Erratum issuedCorrection to2025
Authors and funding
8 authors.
Funding
Abstract
Cardiac fibrosis is the hallmark of cardiovascular disease (CVD), which is leading cause of death worldwide. Previously, we have shown that interleukin-10 (IL10) reduces pressure overload (PO)-induced cardiac fibrosis by inhibiting the recruitment of bone marrow fibroblast progenitor cells (FPCs) to the heart. However, the precise mechanism of FPC involvement in cardiac fibrosis remains unclear. Recently, exosomes and small extracellular vesicles (sEVs) have been linked to CVD progression. Thus, we hypothesized that pro-fibrotic miRNAs enriched in sEV-derived from IL10 KO FPCs promote cardiac fibrosis in pressure-overloaded myocardium. Small EVs were isolated from FPCs cultured media and characterized as per MISEV-2018 guidelines. Small EV's miRNA profiling was performed using Qiagen fibrosis-associated miRNA profiler kit. For functional analysis, sEVs were injected in the heart following TAC surgery. Interestingly, TGFβ-treated IL10-KO-FPCs sEV increased profibrotic genes expression in cardiac fibroblasts. The exosomal miRNA profiling identified miR-21a-5p as the key player, and its inhibition with antagomir prevented profibrotic signalling and fibrosis. At mechanistic level, miR-21a-5p binds and stabilizes
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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 Socratic graph.