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

Jamie Francisco, Yu Zhang, Jae Im Jeong, Wataru Mizushima, Shohei Ikeda, Andreas Ivessa, Shinichi Oka, Peiyong Zhai, Michelle D. Tallquist, Dominic P. Del Re

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)931-945
Number of pages15
JournalJACC: Basic to Translational Science
Volume5
Issue number9
DOIs
StatePublished - Sep 2020

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Keywords

  • Hippo signaling
  • YAP
  • cardiac fibrosis
  • heart failure
  • myocardial infarction

Fingerprint Dive into the research topics of 'Blockade of Fibroblast YAP Attenuates Cardiac Fibrosis and Dysfunction Through MRTF-A Inhibition'. Together they form a unique fingerprint.

Cite this