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  1. Home
  3. Fahd1 Prevents Neuronal Ferroptosis By Modulating R-loop And The Cgas-sting Pathway.
  1. Home
  3. Fahd1 Prevents Neuronal Ferroptosis By Modulating R-loop And The Cgas-sting Pathway.

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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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FAHD1 prevents neuronal ferroptosis by modulating R-loop and the cGAS-STING pathway.

Bitao Wang1, Yubiao Yang2, Zhi Zeng2

  • 1Ningbo University Health Science Center, Ningbo, Zhejiang, 315211, China.

Open Medicine (Warsaw, Poland)
|October 3, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

FAHD1 downregulation exacerbates oxidative stress-induced neuronal ferroptosis. Overexpressing FAHD1 protects neurons by reducing R-loop formation and inhibiting the cGAS-STING pathway, offering a potential therapeutic target for neurological disorders.

Keywords:
FAHD1R-loopcGAS–STING pathwayneuronal ferroptosisoxidative stress

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Ferroptosis, a form of iron-dependent cell death, is implicated in neurological disorders like neurodegenerative diseases and CNS injuries.
  • Current therapeutic strategies for these conditions are often ineffective due to complex pathophysiology.
  • The precise mechanisms driving neuronal ferroptosis remain incompletely understood.

Purpose of the Study:

  • To investigate the role of FAHD1 (Fatty Acid Hydroxylase Domain Containing 1) in neuronal ferroptosis.
  • To explore FAHD1's potential as a therapeutic target for neurological conditions.

Main Methods:

  • Bioinformatic analyses and cellular experiments were conducted.
  • Immunofluorescence, dot blot, and western blotting assessed FAHD1's effects on R-loop formation and cGAS-STING pathway proteins.

Main Results:

  • FAHD1 expression was significantly downregulated in primary neurons under oxidative stress.
  • Ferroptosis was identified as a key mechanism in oxidative stress-induced neuronal damage.
  • FAHD1 overexpression reduced reactive oxygen species, R-loop formation, and preserved genomic stability, suppressing ferroptosis via cGAS-STING pathway inhibition.

Conclusions:

  • FAHD1 acts as a critical regulator of neuronal ferroptosis.
  • FAHD1 presents a potential therapeutic target for neurodegenerative diseases and CNS injuries.