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Related Experiment Video

Updated: Feb 23, 2026

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Ascorbic acid promotes a TGFβ1-induced myofibroblast phenotype switch.

Bram Piersma1, Olaf Y Wouters2, Saskia de Rond2

  • 1Department of Pathology and Medical Biology, Matrix research Group, University of Groningen University Medical Center Groningen, Groningen, The Netherlands b.piersma@umcg.nl.

Physiological Reports
|September 15, 2017
PubMed
Summary

Vitamin C (ascorbic acid) regulates myofibroblast behavior beyond collagen synthesis. It enhances myofibroblast contraction and gene expression, independent of Smad2/3 signaling.

Keywords:
Ascorbic acidTGFβ1collagenfibrosismyofibroblast

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • l-Ascorbic acid (vitamin C) is essential for collagen maturation.
  • Its role in myofibroblast phenotype regulation beyond collagen synthesis is not fully understood.

Purpose of the Study:

  • To investigate additional functions of ascorbic acid in regulating myofibroblast phenotype.
  • To explore vitamin C's impact on myofibroblast characteristics beyond collagen biosynthesis.

Main Methods:

  • Assessed TGFβ1-induced gene expression (COL1A1, ACTA2, COL4A1, DDR1, CCN2).
  • Evaluated αSMA stress fiber formation and collagen synthesis/deposition.
  • Measured myofibroblast contraction in a 3D collagen lattice.
  • Investigated the role of Smad2/3 signaling.

Main Results:

  • Ascorbic acid positively influenced TGFβ1-induced expression of COL1A1, ACTA2, and COL4A1.
  • AA promoted αSMA stress fiber formation and collagen type I and IV synthesis/deposition.
  • AA amplified myofibroblast contractile phenotype and increased DDR1 and CCN2 expression.
  • The mechanism of AA action appeared independent of Smad2/3 signaling.

Conclusions:

  • Ascorbic acid plays a significant role in regulating myofibroblast phenotype and function.
  • Vitamin C enhances myofibroblast contractility and gene expression, suggesting broader biological roles.
  • AA's effects on myofibroblasts are mediated through pathways independent of Smad2/3 signaling.