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  4. Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway

Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway

EXPERIMENTAL AND THERAPEUTIC MEDICINE, 2021 · DOI: 10.3892/etm.2021.10700 · Published: July 8, 2021

Spinal Cord InjuryNeurologyGenetics

Simple Explanation

This study investigates how insulin-like growth factor 1 (IGF-1) affects recovery after spinal cord injury (SCI). It focuses on a process called autophagy, where cells recycle damaged parts. The research suggests that IGF-1 helps in recovery by influencing the PI3K/Akt/mTOR pathway, which in turn reduces autophagy. This was shown in both lab-grown cells and in rats with SCI. The findings indicate that IGF-1 could be a potential treatment for SCI by protecting nerve cells and improving their function, possibly through the PI3K/Akt/mTOR signaling pathway.

Study Duration
4 Weeks
Participants
24 Sprague-Dawley rats, SH-SY5Y neuroblastoma cells
Evidence Level
Level II; In vitro and in vivo study

Key Findings

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    IGF-1 significantly increased cell survival in vitro compared to the control group, suggesting a protective effect on nerve cells.
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    Neurological function was improved in rats with SCI treated with IGF-1 compared to those without treatment, indicating enhanced recovery.
  • 3
    IGF-1 inhibited autophagy by activating the PI3K/Akt/mTOR signaling pathway, both in vitro and in vivo, suggesting a potential mechanism for its neuroprotective effects.

Research Summary

This study aimed to investigate the neuroprotective and autophagic effects of IGF‑1 on SCI, and to determine the role of the PI3K/Akt/mTOR signaling pathway in this process. The results of the present study demonstrated that IGF‑1 promoted functional recovery in SCI rats and increased the number of surviving neural cells following injury in vitro. The IGF‑1‑induced inhibition of autophagy may be associated with activation of the PI3K/Akt/mTOR signaling pathway.

Practical Implications

Potential therapeutic target

IGF-1 shows promise as a therapeutic agent for spinal cord injury due to its neuroprotective effects.

Mechanism-based treatment

The PI3K/Akt/mTOR signaling pathway may be a viable target for SCI treatment strategies.

Clinical accessibility

IGF-1 is already approved by the FDA, facilitating its potential translation into clinical use for SCI treatment.

Study Limitations

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