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WISP-1 Regulates Cardiac Fibrosis by Promoting Cardiac Fibroblasts' Activation and Collagen Processing.

Ze Li1, Helen Williams1, Molly L Jackson1

  • 1Translational Health Sciences, Bristol Medical School, University of Bristol, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.

Cells
|June 19, 2024
PubMed
Summary

Wnt1-inducible signalling pathway protein-1 (WISP-1) drives cardiac fibrosis by activating cardiac fibroblasts and promoting collagen maturation. Blocking WISP-1 in mice reduced hypertension-induced cardiac fibrosis.

Keywords:
WISP-1/CCN4cardiac fibroblastscardiac fibrosiscollagen

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Area of Science:

  • Cardiovascular Biology
  • Fibrosis Research
  • Molecular Medicine

Background:

  • Hypertension causes cardiac fibrosis through fibroblast activation and collagen buildup.
  • The role of Wnt1-inducible signalling pathway protein-1 (WISP-1) in this process is not fully understood.

Purpose of the Study:

  • To investigate if WISP-1 promotes cardiac fibroblast activation and collagen synthesis.
  • To determine WISP-1's role in angiotensin II-induced cardiac fibrosis in vivo.

Main Methods:

  • Human cardiac fibroblasts (HCFs) were treated with WISP-1.
  • WISP-1 wild-type and knockout mice were infused with angiotensin II (AngII).
  • Immunohistochemistry was used to assess collagen deposition and WISP-1's effects.

Main Results:

  • WISP-1 induced cardiac fibroblast phenotypic switching and type I collagen processing.
  • WISP-1 activated Akt phosphorylation via integrin β1 and ADAMTS-2.
  • WISP-1 knockout mice showed reduced AngII-induced cardiac fibrosis and collagen deposition.

Conclusions:

  • WISP-1 is a key mediator of cardiac fibrotic remodelling.
  • WISP-1 promotes cardiac fibroblast activation and collagen maturation via the integrin β1-Akt-ADAMTS-2 pathway.
  • Targeting WISP-1 may offer a therapeutic strategy for clinical treatment of cardiac fibrosis.