Key result
Serum-derived extracellular vesicles containing MIAT promoted atrial fibrosis, inflammation, oxidative stress, and atrial remodeling by abolishing miR-485-5p-mediated CXCL10 inhibition.
Why the study?
The role of lncRNA MIAT enriched in serum-derived extracellular vesicles in atrial fibrillation remained to be elucidated.
Population
AF patients, Ang II-induced mice, and HL-1 cells
Comparison
Ectopic expression vs depletion assays and co-culture with serum-derived EVs
Design
Preclinical in vitro and in vivo mechanistic study
Authors
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Highlights EV-MIAT as AF driver in animal models; leaves open translation to human therapy or targets.
Serum-derived EVs containing lncRNA MIAT promote atrial remodeling and AF via the miR-485-5p/CXCL10 axis, highlighting a potential novel pathophysiological mechanism and therapeutic target.
Chen et al. (2021) studied Atrial fibrillation. Serum-derived extracellular vesicles containing MIAT was evaluated on Atrial fibrosis, inflammation, oxidative stress, and atrial remodeling. Serum-derived extracellular vesicles containing MIAT promoted atrial fibrosis, inflammation, oxidative stress, and atrial remodeling by abolishing miR-485-5p-mediated CXCL10 inhibition.
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