Key result
Endothelial plasticity drives atrial fibrosis and AF, revealing new therapeutic targets.
Endothelial plasticity and endothelial-to-mesenchymal activation contribute to atrial fibrosis, presenting a potential novel therapeutic target for atrial fibrillation.
Endothelial targeting in AF remains investigational; leaves open mechanistic validation and clinical translation.
Endothelial plasticity contributes to atrial fibrosis through endothelial-to-mesenchymal activation (EndMA) and paracrine transforming growth factor-beta 1 (TGF-β1) signalling, promoting fibroblast activation and excessive extracellular matrix (ECM) deposition. This endothelial-driven fibrotic remodelling establishes a substrate for the initiation and perpetuation of atrial fibrillation (AF), highlighting endothelial cells (ECs) as targets for novel therapeutic strategies.
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Luxán et al. (2025) conducted a review in Atrial fibrillation. Endothelial plasticity and endothelial-to-mesenchymal activation contribute to atrial fibrosis and atrial fibrillation, highlighting endothelial cells as potential targets for novel therapies.
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