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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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ROP16 Promotes Epithelial-Mesenchymal Transition-Like Changes in Ocular Toxoplasmosis via STAT3 and TGF-β1 Pathways.

Lingling Song1, Lihui Xu1,2, Yao Liu1

  • 1Department of Microbiology and Parasitology, Anhui Provincial Key Laboratory of Zoonoses, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China, ahmu.edu.cn.

Transboundary and Emerging Diseases
|May 25, 2026
PubMed
Summary

Toxoplasma gondii infection causes ocular toxoplasmosis (OT) by inducing epithelial-mesenchymal transition (EMT)-like changes. The parasite protein ROP16 activates STAT3 and TGF-β1 pathways, offering potential therapeutic targets for vision-threatening OT.

Keywords:
EMT-like changesOTROP16STAT3TGF-β1Toxoplasma gondii

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Area of Science:

  • Ophthalmology
  • Infectious Diseases
  • Cell Biology

Background:

  • Toxoplasmosis, caused by *Toxoplasma gondii*, affects one-third of the global population.
  • Ocular toxoplasmosis (OT) is a significant cause of vision loss, with poorly understood pathogenesis.
  • Current therapies for OT are limited and not targeted effectively.

Purpose of the Study:

  • To elucidate the pathogenic mechanisms of ocular toxoplasmosis.
  • To investigate the role of *Toxoplasma gondii* rhoptry protein 16 (ROP16) in OT.
  • To identify potential therapeutic targets for OT.

Main Methods:

  • Induction of epithelial-mesenchymal transition (EMT)-like changes in human RPE cells and murine ocular tissues by *T. gondii*.
  • Utilized ROP16 knockout and overexpression parasite models for mechanistic studies.
  • Investigated the involvement of STAT3 and TGF-β1 signaling pathways.
  • Administered pharmacological inhibitors of STAT3 and TGF-β1 in vitro and in vivo models.

Main Results:

  • *T. gondii* infection induced EMT-like changes in RPE cells and ocular tissues.
  • Parasite protein ROP16 was identified as a key mediator, promoting EMT-like changes.
  • ROP16 activates the host STAT3 and TGF-β1 signaling pathways.
  • Inhibition of STAT3 or TGF-β1 attenuated EMT-like changes and ameliorated OT pathology in mice.

Conclusions:

  • The ROP16-STAT3 and TGF-β1 signaling axis is crucial in the pathogenesis of ocular toxoplasmosis.
  • This study provides novel insights into OT disease mechanisms.
  • STAT3 and TGF-β1 inhibitors represent promising therapeutic strategies for ocular toxoplasmosis.