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

Research output: Contribution to journal › Letter › Research › peer-review

Standard

TGF-β1-induced endothelial-mesenchymal transition : a potential contributor to fibrotic remodeling in atrial fibrillation? / Saljic, Arnela; Grandi, Eleonora; Dobrev, Dobromir.

In: The Journal of Clinical Investigation, Vol. 132, No. 13, e161070, 2022.

Research output: Contribution to journal › Letter › Research › peer-review

Harvard

Saljic, A, Grandi, E & Dobrev, D 2022, 'TGF-β1-induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?', The Journal of Clinical Investigation, vol. 132, no. 13, e161070. https://doi.org/10.1172/JCI161070

APA

Saljic, A., Grandi, E., & Dobrev, D. (2022). TGF-β1-induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation? The Journal of Clinical Investigation, 132(13), [e161070]. https://doi.org/10.1172/JCI161070

Vancouver

Saljic A, Grandi E, Dobrev D. TGF-β1-induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation? The Journal of Clinical Investigation. 2022;132(13). e161070. https://doi.org/10.1172/JCI161070

Author

Saljic, Arnela ; Grandi, Eleonora ; Dobrev, Dobromir. / TGF-β1-induced endothelial-mesenchymal transition : a potential contributor to fibrotic remodeling in atrial fibrillation?. In: The Journal of Clinical Investigation. 2022 ; Vol. 132, No. 13.

Bibtex

@article{d6b21d7ed4164ed2a990ff724d44d872,
title = "TGF-β1-induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?",
abstract = "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.",
keywords = "EXTRACELLULAR-MATRIX, CARDIAC FIBROBLAST, DISEASE",
author = "Arnela Saljic and Eleonora Grandi and Dobromir Dobrev",
year = "2022",
doi = "10.1172/JCI161070",
language = "English",
volume = "132",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "American Society for Clinical Investigation",
number = "13",

}

RIS

TY - JOUR

T1 - TGF-β1-induced endothelial-mesenchymal transition

T2 - a potential contributor to fibrotic remodeling in atrial fibrillation?

AU - Saljic, Arnela

AU - Grandi, Eleonora

AU - Dobrev, Dobromir

PY - 2022

Y1 - 2022

N2 - 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.

AB - 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.

KW - EXTRACELLULAR-MATRIX

KW - CARDIAC FIBROBLAST

KW - DISEASE

U2 - 10.1172/JCI161070

DO - 10.1172/JCI161070

M3 - Letter

C2 - 35775488

AN - SCOPUS:85133289594

VL - 132

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 13

M1 - e161070

ER -

ID: 313883514