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Updated: Feb 8, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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Thymosin β4 suppresses CCl4 -induced murine hepatic fibrosis by down-regulating transforming growth factor β

Hanchao Li1, Qian Li1, Xueting Zhang2

  • 1Department of Rheumatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.

The Journal of Gene Medicine
|July 5, 2018
PubMed
Abstract

Insights

Thymosin beta4 (Tβ4) shows significant anti-fibrotic effects in mouse liver fibrosis by reducing collagen and HSC activation. This action is linked to down-regulating TGF-β receptor-II, thus inhibiting fibrotic signaling.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Biochemistry

Background:

  • Liver fibrosis is a significant health concern characterized by excessive extracellular matrix deposition.
  • Hepatic stellate cells (HSCs) play a central role in liver fibrosis progression.
  • Thymosin beta4 (Tβ4) is a key actin-sequestering protein with potential therapeutic roles.

Purpose of the Study:

  • To investigate the therapeutic effects of thymosin beta4 (Tβ4) on carbon tetrachloride (CCl4)-induced liver fibrosis in mice.
  • To elucidate the underlying molecular mechanisms by which Tβ4 exerts its anti-fibrotic actions.

Main Methods:

  • Quantitative real-time PCR and immunohistochemistry were used to assess Tβ4 expression in fibrotic liver tissues.
  • Adeno-associated virus-mediated Tβ4 (AAV-Tβ4) delivery was employed to evaluate its effects on CCl4-induced liver fibrosis.
  • In vitro studies using HSCs and hepatocytes were conducted to confirm Tβ4's direct effects.

Main Results:

  • Tβ4 expression was decreased in fibrotic livers but increased upon acute CCl4 injury.
  • AAV-Tβ4 pre-treatment significantly reduced liver injury, collagen deposition, HSC activation, and pro-fibrotic cytokine expression (TGF-β1, PDGF-B, CTGF, PAI-1).
  • In vitro, Tβ4 suppressed HSC proliferation, inhibited TGF-β1-induced HSC activation, and reduced TGF-β1-induced pro-fibrotic gene expression.

Conclusions:

  • Tβ4 demonstrates potent anti-fibrotic activity in the liver.
  • The anti-fibrotic effects of Tβ4 are mediated, at least in part, by down-regulating TGF-β receptor-II (TGF-βRII).
  • This down-regulation of TGF-βRII by Tβ4 effectively blunts TGF-β1-mediated fibrogenetic signaling in HSCs and hepatocytes.
Keywords:
TGF-β receptor-IIadeno-associated virushepatic fibrosismicethymosin β4

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