2026-06-14T06:44:33Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/79812024-09-27T08:34:33Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Panse, Kalyani D
author
Felkin, Leanne E
author
Lopez-Olaneta, Marina
author
Gomez-Salinero, Jesus M.
author
Villalba-Orero, Maria
author
Munoz, Lucia
author
Nakamura, Kazuto
author
Shimano, Masayuki
author
Walsh, Kenneth
author
Barton, Paul J R
author
Rosenthal, Nadia
author
Lara-Pezzi, Enrique
funder
British Heart Foundation
funder
National Institute for Health Research (Reino Unido)
funder
South London and Maudsley NHS Foundation Trust (Reino Unido)
funder
Imperial College London (Reino Unido)
funder
Unión Europea. Comisión Europea
funder
Ministerio de Ciencia e Innovación (España)
funder
Comunidad de Madrid (España)
2019-07-29T13:05:32Z
2019-07-29T13:05:32Z
2012-12
J Cardiovasc Transl Res. 2012; 5(6):814-26
10.1007/s12265-012-9400-9
1937-5395
1937-5387
Journal of cardiovascular translational research
22915069
http://hdl.handle.net/20.500.12105/7981
Follistatins are extracellular inhibitors of the TGF-β 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.
eng
Follistatin-like 3 mediates paracrine fibroblast activation by cardiomyocytes
journal article
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https://repisalud.isciii.es/bitstreams/61d7dc2c-5601-4f34-bcd3-8a4468377109/download
File
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application/pdf
FollistatinLike3MediatesParacrine_2012.pdf
URL
https://repisalud.isciii.es/bitstreams/cf16ff51-cb76-4a01-8af7-7358dbd082bf/download
File
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text/plain
FollistatinLike3MediatesParacrine_2012.pdf.txt