RT Journal Article
T1 Follistatin-Like 3 Mediates Paracrine Fibroblast Activation by Cardiomyocytes
A1 Panse, Kalyani D.
A1 Felkin, Leanne E.
A1 López-Olañeta, Marina M.
A1 Gómez-Salinero, Jesús
A1 Muñoz, Lucía
A1 Nakamura, Kazuto
A1 Shimano, Masayuki
A1 Walsh, Kenneth
A1 Barton, Paul J. R.
A1 Rosenthal, Nadia
A1 Lara-Pezzi, Enrique
A1 Villalba Orero, María
AB Follistatins are extracellular inhibitors of the TGF-beta family ligands including activin A, myostatin and bone morphogenetic proteins. Follistatin-like 3 (FSTL3) is a potent inhibitor of activin signalling and antagonises the cardioprotective role of activin A in the heart. FSTL3 expression is elevated in patients with heart failure and is upregulated in cardiomyocytes by hypertrophic stimuli, but its role in cardiac remodelling is largely unknown. Here, we show that the production of FSTL3 by cardiomyocytes contributes to the paracrine activation of cardiac fibroblasts, inducing changes in cell adhesion, promoting proliferation and increasing collagen production. We found that FSTL3 is necessary for this response and for the induction of cardiac fibrosis. However, full activation requires additional factors, and we identify connective tissue growth factor as a FSTL3 binding partner in this process. Together, our data unveil a novel mechanism of paracrine communication between cardiomyocytes and fibroblasts that may provide potential as a therapeutic target in heart remodelling.
PB Springer
SN 1937-5387
SN 1937-5395
YR 2012
FD 2012-08-23
LK https://hdl.handle.net/20.500.14352/95605
UL https://hdl.handle.net/20.500.14352/95605
LA eng
NO British Heart Foundation
NO Unión Europea
NO Ministerio de Ciencia e Innovación
NO Comunidad de Madrid
DS Docta Complutense
RD 21 abr 2025