ArticleClinical and translational medicine2021
Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR-485-5p-mediated CXCL10 inhibition.
Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 44 citations in OpenAlex.
- The Defect of iNKT Cells Mediates Mitochondrial Dysfunction Through IL-6/STAT3 Signaling to Induce Atrial Inflammation and Fibrosis to Aggravate Postoperative Atrial Fibrillation.Physiological research · 2026Article
- Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- The long non-coding RNA PVT1 promotes keratinocyte proliferation and inflammation in psoriasis by targeting miR-485-5p.Journal of molecular histology · 2026Article
- MIAT: An important long non-coding RNA regulating cardiovascular and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2026Review
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Role of ncRNAs in Neurological Disorders and Cardiovascular Diseases.Experientia supplementum (2012) · 2026Review
- The multifaceted roles of non-coding RNAs in cell-cell communication in cardiovascular health and disease.Cell & bioscience · 2025Review
- Transferrin receptor knockdown attenuates atrial fibrillation by inhibiting cardiomyocyte ferroptosis and atrial fibrosis.Experimental animals · 2025Article
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- Long Non-coding RNA Involved in the Pathophysiology of Atrial Fibrillation.Cardiovascular drugs and therapy · 2025Review
- Exosomal lncRNA XR_001793654.1 in human cardiac explant-derived alleviates atrial fibrillation via abolishing the miR-107-3p-mediated KLF13 inhibition.Frontiers in cell and developmental biology · 2025Article
- Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025Review
- Article
- Inflammation in liver fibrosis and atrial fibrillation: A prospective population-based proteomic study.JHEP reports : innovation in hepatology · 2024Article
- Extracellular Vesicle-Derived Non-Coding RNAs: Key Mediators in Remodelling Heart Failure.Current issues in molecular biology · 2024Review
- Regulatory axis of circular RNA DTNB, microRNA-485-5p, and myeloid cell leukemia 1 attenuates inflammation and apoptosis in caerulein-treated AR42J cells.Functional & integrative genomics · 2024Article
- Article
- Administration of USP7 inhibitor p22077 alleviates Angiotensin II (Ang II)-induced atrial fibrillation in Mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Review
- Circulating extracellular vesicles as biomarkers in the diagnosis, prognosis and therapy of cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtrial fibrillation (AF), a supraventricular arrhythmia that impairs cardiac function, is a main source of morbidity and mortality. Serum-derived extracellular vesicles (EVs) have been identified to carry potential biomarker or target for the diagnosis and treatment of AF. We intended to dissect out the role of lncRNA MIAT enriched in serum-derived EVs in AF.
methodsMIAT expression was quantified in EVs isolated from serum samples of AF patients. Mouse and cell models of AF were developed after angiotensin II (Ang II) induction. Relationship between MIAT, miR-485-5p, and CXCL10 was identified. Ectopic expression and depletion assays were implemented in Ang II-treated mice or HL-1 cells, or those co-cultured with serum-derived EVs to explore the roles of EV-carried MIAT.
resultsMIAT was upregulated in EVs from serum samples of AF patients. Further analysis indicated that MIAT enriched in serum-derived EVs promoted atrial fibrosis, inflammation and oxidative stress, and aggravated the atrial remodeling and resultant AF. Mechanistically, MIAT bound to miR-485-5p and weakened its inhibitory role on the target CXCL10, which was responsible for the role of serum-derived EV containing MIAT in cellular fibrosis, oxidative stress and inflammation, and atrial remodeling in vivo.
conclusionsIn conclusion, serum-derived EV containing MIAT facilitates atrial remodeling and exacerbates the AF by abolishing the miR-485-5p-mediated CXCL10 inhibition. This finding aids in the deeper understanding about the pathophysiology of AF.
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