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MiR-181b targets semaphorin 3a to mediate TGF-β-induced endothelial-to-mesenchymal transition related to atrial fibrillation

ABSTRACT: Background:This study investigated if and how atrial endothelial cells may transform to mesenchymal cells and contribute to atrial fibrosis via endothelial-to-mesenchymal transition (EndMT). Results:We show a novel mechanistic link between TGF-β1/SMAD signaling and decreased Sema3a expression through the induction of miR-181b; this pathway plays an important role in EndMT associated with the pathogenesis of AF. Both miR-181b and Sema3a are potential therapeutic targets in AF.

ORGANISM(S): Mus musculus

PROVIDER: GSE201318 | GEO | 2022/04/27

REPOSITORIES: GEO

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MiR-181b Targets Semaphorin 3a to Mediate TGF-β-induced Endothelial to Mesenchymal Transition: Implication in Atrial Fibrillation

Project description:Background:This study investigated if and how atrial endothelial cells may transform to mesenchymal cells and contribute to atrial fibrosis via endothelial-to-mesenchymal transition (EndMT). Results:We show a novel mechanistic link between TGF-β1/SMAD signaling and decreased Sema3a expression through the induction of miR-181b; this pathway plays an important role in EndMT associated with the pathogenesis of AF. Both miR-181b and Sema3a are potential therapeutic targets in AF.

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MiR-181b targets semaphorin 3a to mediate TGF-β-induced endothelial-to-mesenchymal transition related to atrial fibrillation

Project description:MiR-181b targets semaphorin 3a to mediate TGF-β-induced endothelial-to-mesenchymal transition related to atrial fibrillation

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