Fibroblast growth factor 21 inhibits ferroptosis following spinal cord injury by regulating heme oxygenase-1

Neural Regeneration Research, 2024 · DOI: https://doi.org/10.4103/1673-5374.387979 · Published: November 8, 2023

Simple Explanation

Spinal cord injury (SCI) can lead to lower limb dysfunction and death. Secondary injuries like ferroptosis, a cell death cascade, exacerbate the initial damage. Interfering with the ferroptosis pathway is a new strategy for the treatment of SCI. Fibroblast growth factor 21 (FGF21) is a protein that can prevent metabolic disorders and has neuroprotective effects. It can inhibit neuronal death and promote axon elongation after SCI. Heme oxygenase-1 (HO-1) is an enzyme involved in iron metabolism. This study found that FGF21 inhibits ferroptosis after SCI by downregulating HO-1.

Study Duration

28 days

Participants

140 adult, male Sprague-Dawley rats

Evidence Level

Not specified

Key Findings

1
FGF21 levels decrease in spinal cord tissue after SCI, while ferroptosis is aggravated.
2
HO-1 expression increases rapidly after SCI, and HO-1 aggravates ferroptosis after SCI.
3
FGF21 inhibits ferroptosis by downregulating HO-1, suggesting a potential treatment for SCI.

Research Summary

This study investigates the role of fibroblast growth factor 21 (FGF21) in ferroptosis following spinal cord injury (SCI) in rats. The study found that FGF21 levels decrease after SCI, while heme oxygenase-1 (HO-1) expression increases, leading to aggravated ferroptosis. The results indicate that FGF21 inhibits ferroptosis by downregulating HO-1, suggesting a potential therapeutic strategy for SCI.

Practical Implications

Therapeutic Potential

Activation of fibroblast growth factor 21 may provide a potential treatment for spinal cord injury.

Mechanistic Understanding

These findings could provide a new potential mechanistic explanation for fibroblast growth factor 21 in the treatment of spinal cord injury.

Drug Development

rhFGF21 treatment can inhibit SCI-induced ferroptosis by suppressing iron accumulation in spinal cord tissue, and thereby improve motor neuron survival and neurofunctional recovery.

Study Limitations

1
Lack of intuitive quantification by immunohistochemistry for FGF21 and HO-1.
2
Subjective assessment of functional recovery due to lack of video analysis of joint kinematics.
3
The molecular mechanism by which FGF21 induces the downregulation of HO-1 requires further investigation.

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