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Pre-eclampsia-related TLR2/4 signaling activates NOX2/4 to induce oxidative stress and ferroptosis in trophoblasts.

Yan Zhang1, Yunmei Ke2, Baosheng Zhu1

  • 1Department of Medical Genetics, Yunnan Provincial Key Laboratory of Birth Defects and Genetic Diseases, NHC Key Laboratory of Healthy Birth and Birth Defect Prevention in Western China, The First People's Hospital of Yunnan Province/The Affiliated Hospital of Kunming University of Science and Technology, Kunming University of Science and Technology, No. 157 Jinbi Road, Xishan District, Kunming, Yunnan, China.

European Journal of Medical Research
|December 16, 2025
PubMed
Summary

Toll-like receptor (TLR) signaling drives oxidative stress and ferroptosis in pre-eclampsia (PE) placentas. Targeting TLR signaling offers a potential therapeutic strategy to improve trophoblast function and ameliorate PE symptoms.

Keywords:
FerroptosisOxidative stressPre-eclampsiaToll-like receptor (TLR)Trophoblasts

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Area of Science:

  • Reproductive biology
  • Immunology
  • Cellular pathology

Background:

  • Oxidative stress and ferroptosis are implicated in trophoblast dysfunction in pre-eclampsia (PE).
  • Toll-like receptor (TLR) signaling pathways are investigated for their role in PE-related placental pathology.

Purpose of the Study:

  • To investigate the role of TLR signaling in PE-induced ferroptosis.
  • To explore the therapeutic potential of targeting TLR signaling in a PE animal model.

Main Methods:

  • Analysis of placental tissues from PE patients and controls for TLR2/4 and MAPK signaling.
  • In vitro study using HTR-8/SVneo trophoblasts subjected to hypoxia/reoxygenation (H/R).
  • In vivo study using a reduced uterine perfusion pressure (RUPP) rat model of PE, treated with TLR2/4 or NADPH oxidase (NOX) inhibitors.

Main Results:

  • Upregulated TLR2/4 and activated MAPK signaling observed in PE placentas and H/R trophoblasts.
  • Inhibition of TLR2/4 improved trophoblast function and reduced ferroptosis markers.
  • Targeting TLR2/4 and NOX ameliorated PE syndromes in the rat model, including reduced blood pressure and proteinuria.

Conclusions:

  • TLR2/4-dependent oxidative stress and ferroptosis contribute to trophoblast dysfunction in PE.
  • Targeting TLR signaling offers a promising intervention strategy for pre-eclampsia.