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

J Clin Invest. 2022 Jul 1;132(13):e161070. doi: 10.1172/JCI161070.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Atrial Fibrillation* / pathology
  • Epithelial-Mesenchymal Transition
  • Fibroblasts / pathology
  • Fibrosis / pathology
  • Heart Atria / pathology
  • Humans
  • Myocardium* / pathology
  • Transforming Growth Factor beta1* / metabolism

Substances

  • TGFB1 protein, human
  • Transforming Growth Factor beta1