ArticleJournal of translational medicine2022
Atrial myocyte-derived exosomal microRNA contributes to atrial fibrosis in atrial fibrillation.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The Origin and Application of Cardiomyocyte-Derived Small Extracellular Vesicles: A Systematic Review.International journal of medical sciences · 2026Pooled it
- Metabolic Signatures of Atrial Functional Impairment in Paroxysmal Atrial Fibrillation Patients: A CMR Strain-metabolomics Study.Journal of cardiovascular translational research · 2026Article
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.Reviews in cardiovascular medicine · 2026Review
- MicroRNA profile in normal pregnancies with isolated low IgM anticardiolipin levels.Reproduction & fertility · 2026Article
- Extracellular Vesicles as Biomarkers and Non-Surgical Therapeutics in Cardiovascular Diseases.Journal of clinical medicine · 2026Review
- Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.Cardiovascular therapeutics · 2026Article
- Targeted nanodelivery strategies for atrial fibrillation: concomitant targeting of fibrosis suppression and electrical conduction restoration through advanced nanobiotechnology.Journal of nanobiotechnology · 2025Review
- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- GPD1L as a potential biomarker associated with Treg cell infiltration and lipid metabolism in clear cell renal cell carcinoma.Journal of translational medicine · 2025Article
- Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025Review
- Exosome-Based Therapy in Cardiovascular Diseases: A New Frontier in Cardiovascular Disease Treatment.Korean circulation journal · 2025Review
- miR-210 overexpression increases pressure overload-induced cardiac fibrosis.Non-coding RNA research · 2025Article
- Role of Exosomes in Cardiovascular Disease: A Key Regulator of Intercellular Communication in Cardiomyocytes.ACS omega · 2025Review
- Associations of microRNA Gene Polymorphisms With Salt Sensitivity, Longitudinal Blood Pressure Changes, and Hypertension Incidence in the Chinese Population.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- The role of complement C1q in atrial fibrillation: a marker for disease progression and surgical outcomes.Frontiers in cardiovascular medicine · 2025Article
- Adipose stem cell-derived exosomes circular RNA circFryl attenuate atrial fibrosis and cardiomyocyte apoptosis in atrial fibrillation.Iranian journal of basic medical sciences · 2025Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtrial fibrosis plays a critical role in the development of atrial fibrillation (AF). Exosomes are a promising cell-free therapeutic approach for the treatment of AF. The purposes of this study were to explore the mechanisms by which exosomes derived from atrial myocytes regulate atrial remodeling and to determine whether their manipulation facilitates the therapeutic modulation of potential fibrotic abnormalities during AF.
methodsWe isolated exosomes from atrial myocytes and patient serum, and microRNA (miRNA) sequencing was used to analyze exosomal miRNAs in exosomes derived from atrial myocytes and patient serum. mRNA sequencing and bioinformatics analyses corroborated the key genes that were direct targets of miR-210-3p.
resultsThe miRNA sequencing analysis identified that miR-210-3p expression was significantly increased in exosomes from tachypacing atrial myocytes and serum from patients with AF. In vitro, the miR-210-3p inhibitor reversed tachypacing-induced proliferation and collagen synthesis in atrial fibroblasts. Accordingly, miR-210-3p knock out (KO) reduced the incidence of AF and ameliorated atrial fibrosis induced by Ang II. The mRNA sequencing analysis and dual-luciferase reporter assay showed that glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is a potential target gene of miR-210-3p. The functional analysis suggested that GPD1L regulated atrial fibrosis via the PI3K/AKT signaling pathway. In addition, silencing GPD1L in atrial fibroblasts induced cell proliferation, and these effects were reversed by a PI3K inhibitor (LY294002).
conclusionsAtrial myocyte-derived exosomal miR-210-3p promoted cell proliferation and collagen synthesis by inhibiting GPD1L in atrial fibroblasts. Preventing pathological crosstalk between atrial myocytes and fibroblasts may be a novel target to ameliorate atrial fibrosis in patients with AF.
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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.