TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?

Atrial fibrillation (AF) is the most common cardiac arrhythmia worldwide, with an unmet therapeutic need. Fibrotic remodeling, in which collagen-producing atrial fibroblasts play a crucial role, substantially contributes to arrhythmia promotion and progression. In this issue of the JCI, Lai, Tsai, a...

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Main Authors: Arnela Saljic, Eleonora Grandi, Dobromir Dobrev
Format: Article
Language:English
Published: American Society for Clinical Investigation 2022-07-01
Series:The Journal of Clinical Investigation
Online Access:https://doi.org/10.1172/JCI161070
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author Arnela Saljic
Eleonora Grandi
Dobromir Dobrev
author_facet Arnela Saljic
Eleonora Grandi
Dobromir Dobrev
author_sort Arnela Saljic
collection DOAJ
description Atrial fibrillation (AF) is the most common cardiac arrhythmia worldwide, with an unmet therapeutic need. Fibrotic remodeling, in which collagen-producing atrial fibroblasts play a crucial role, substantially contributes to arrhythmia promotion and progression. In this issue of the JCI, Lai, Tsai, and co-authors reveal that TGF-β1 promoted endothelial-mesenchymal transition during AF and put forward the notion that, in the adult heart, atrial fibroblasts can originate from different cellular sources. These important findings extend our understanding of the origin, biology, and function of fibroblasts and offer possibilities for therapeutic targeting of fibrosis in AF.
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spelling doaj.art-bc621f7b4af44821a1931fbc9b91b0052022-12-22T03:33:11ZengAmerican Society for Clinical InvestigationThe Journal of Clinical Investigation1558-82382022-07-0113213TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?Arnela SaljicEleonora GrandiDobromir DobrevAtrial fibrillation (AF) is the most common cardiac arrhythmia worldwide, with an unmet therapeutic need. Fibrotic remodeling, in which collagen-producing atrial fibroblasts play a crucial role, substantially contributes to arrhythmia promotion and progression. In this issue of the JCI, Lai, Tsai, and co-authors reveal that TGF-β1 promoted endothelial-mesenchymal transition during AF and put forward the notion that, in the adult heart, atrial fibroblasts can originate from different cellular sources. These important findings extend our understanding of the origin, biology, and function of fibroblasts and offer possibilities for therapeutic targeting of fibrosis in AF.https://doi.org/10.1172/JCI161070
spellingShingle Arnela Saljic
Eleonora Grandi
Dobromir Dobrev
TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
The Journal of Clinical Investigation
title TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
title_full TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
title_fullStr TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
title_full_unstemmed TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
title_short TGF-β1–induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
title_sort tgf β1 induced endothelial mesenchymal transition a potential contributor to fibrotic remodeling in atrial fibrillation
url https://doi.org/10.1172/JCI161070
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AT eleonoragrandi tgfb1inducedendothelialmesenchymaltransitionapotentialcontributortofibroticremodelinginatrialfibrillation
AT dobromirdobrev tgfb1inducedendothelialmesenchymaltransitionapotentialcontributortofibroticremodelinginatrialfibrillation