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  4. FGF1 improves functional recovery through inducing PRDX1 to regulate autophagy and anti-ROS after spinal cord injury

FGF1 improves functional recovery through inducing PRDX1 to regulate autophagy and anti-ROS after spinal cord injury

J Cell Mol Med, 2018 · DOI: 10.1111/jcmm.13566 · Published: May 1, 2018

Spinal Cord InjuryNeurologyGenetics

Simple Explanation

This study investigates the effects of Fibroblast Growth Factor 1 (FGF1) on spinal cord injury (SCI) recovery. FGF1 has shown promise in protecting and regenerating neurons after SCI, but its use is limited by its instability and inability to cross the blood-spinal cord barrier. The researchers used an adeno-associated virus (AAV) to deliver FGF1 to the spinal cord after injury. They found that this method reduced tissue loss, protected neurons, improved tissue recovery, and promoted axon regeneration and remyelination. The study suggests that FGF1 improves functional recovery after SCI by inducing the expression of PRDX1, an antioxidant protein. This, in turn, increases autophagy (a cellular cleaning process) and reduces reactive oxygen species (ROS), which contribute to secondary injury after SCI.

Study Duration
14 days
Participants
80 adult female Sprague Dawley rats
Evidence Level
Not specified

Key Findings

  • 1
    Overexpression of FGF1 via AAV delivery reduces tissue loss and protects neurons after spinal cord injury.
  • 2
    FGF1 promotes axon regeneration and remyelination in vivo and in vitro.
  • 3
    FGF1 induces PRDX1 expression, which increases autophagy and reduces ROS levels after SCI.

Research Summary

This study investigates the therapeutic potential of FGF1 in treating spinal cord injury (SCI) by delivering FGF1 using an adeno-associated virus (AAV) vector. The results demonstrate that AAV-mediated FGF1 overexpression significantly improves functional recovery after SCI by reducing tissue damage, protecting neurons, and promoting axon regeneration and remyelination. The study identifies a key mechanism through which FGF1 exerts its beneficial effects: by inducing the expression of PRDX1, an antioxidant protein, which in turn regulates autophagy and reduces reactive oxygen species (ROS) levels.

Practical Implications

Therapeutic Target

PRDX1 could be a therapeutic target for SCI.

Delivery Method

AAV vector is an effective delivery strategy for FGF1.

Clinical Applications

The findings may provide insights into the clinical application of FGF1 for acute and chronic SCI patients.

Study Limitations

  • 1
    The exact target and the route for PRDX1 action on the autophagy pathway remain elusive.
  • 2
    The study focused on female rats, limiting generalization to males.
  • 3
    Long-term effects of AAV-FGF1 delivery were not assessed.

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