Blockade of Fibroblast YAP Attenuates Cardiac Fibrosis and Dysfunction Through MRTF-A Inhibition

Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction–in...

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Detalles Bibliográficos
Autores principales: Francisco, Jamie, Zhang, Yu, Jeong, Jae Im, Mizushima, Wataru, Ikeda, Shohei, Ivessa, Andreas, Oka, Shinichi, Zhai, Peiyong, Tallquist, Michelle D., Del Re, Dominic P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Preclinical Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7524792/
https://www.ncbi.nlm.nih.gov/pubmed/33015415
http://dx.doi.org/10.1016/j.jacbts.2020.07.009
Descripción
Sumario:Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction–induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure.

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