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Angiotensin II Activates Yes-Associated Protein (YAP) in Fibroblast Promoting Deep Fascia Remodeling.

Brasilina Caroccia1, Ilaria Caputo1, Giovanni Bertoldi1

  • 1Department of Medicine-DIMED, University of Padova, 35128 Padova, Italy.

International Journal of Molecular Sciences
|November 27, 2025
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Summary

The deep fascia is biologically active, with Angiotensin II (Ang II) activating the YAP pathway in fibroblasts. This Ang II-YAP signaling promotes fibrosis, offering new therapeutic targets for fascial conditions.

Keywords:
Ang II type 1 receptorangiotensin IIfasciafibroblastsremodellingthoracolumbar fasciayes associated protein (YAP)

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Area of Science:

  • Biomedical Science
  • Cell Biology
  • Connective Tissue Research

Background:

  • Deep fascia was historically viewed as passive connective tissue.
  • Emerging evidence highlights its active role in biochemical and biomechanical signaling.
  • Fascia influences proprioception, pain, force transmission, and adaptation to mechanical load.

Purpose of the Study:

  • To investigate the interaction between Angiotensin II (Ang II) signaling and the Yes-associated protein (YAP) mechanosensor in human fascial fibroblasts.
  • To elucidate the role of the Angiotensin type 1 receptor (AT1R) in mediating these effects.
  • To explore the potential of targeting this pathway for fibrotic conditions.

Main Methods:

  • Human fascial fibroblasts were treated with Ang II.
  • YAP activation was assessed via phosphorylation and nuclear translocation.
  • Gene expression of fibrosis-related markers (COL1A1, COL3A1, HABP2) was quantified.
  • Fibroblast proliferation and migration assays were performed.
  • Effects were evaluated with AT1R antagonist (irbesartan) and YAP inhibitor (verteporfin).

Main Results:

  • AT1R was confirmed as the predominant Ang II receptor subtype in fascial fibroblasts.
  • Short-term Ang II exposure activated YAP signaling.
  • Prolonged Ang II treatment significantly upregulated fibrosis-related genes.
  • Ang II promoted fibroblast proliferation and migration via AT1R-dependent pathways.
  • Inhibition of AT1R or YAP attenuated Ang II-induced fibrotic gene expression.

Conclusions:

  • Angiotensin II acts as a key signaling molecule in the deep fascia, influencing fibroblast behavior.
  • A novel Ang II-YAP signaling pathway in fascial fibroblasts promotes fibrotic remodeling.
  • This pathway represents a potential therapeutic target for fascial fibrosis and related disorders.