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Mechanisms, translational opportunities for diabetic polyneuropathy
Honyi Ong1, Mingyang Hong1, Douglas W Zochodne1
1Division of Neurology, Department of Medicine, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada.
Frontiers in Endocrinology
|August 7, 2026
Summary
Diabetic polyneuropathy (DPN) damages sensory nerves in diabetes, causing pain and loss of sensation. Current treatments are limited, but research into nerve regeneration pathways offers future therapeutic hope.
Area of Science:
- Neurology
- Endocrinology
- Regenerative Medicine
Background:
- Diabetic polyneuropathy (DPN) is a frequent complication of diabetes mellitus (DM).
- Peripheral sensory axons are primary targets, leading to sensory loss, pain, and reduced quality of life.
- Current therapeutic options to reverse or halt DPN are unavailable.
Purpose of the Study:
- To review the current understanding of DPN mechanisms.
- To explore novel therapeutic approaches for DPN treatment.
- To identify potential targets for promoting sensory axon resilience and regrowth.
Main Methods:
- Literature review of current DPN mechanisms.
- Analysis of potential new therapeutic targets.
- Exploration of regenerative pathways for nerve repair.
Main Results:
- DPN involves sensory axon degeneration, distal sensory terminal retraction, and failed regenerative repair.
- Abnormalities like insulin signaling and mitochondrial dysfunction contribute to DPN.
- Many potential therapeutic targets require further investigation in DM models and clinical trials.
Conclusions:
- Effective DPN therapies are lacking.
- Regenerative pathways present a promising future strategy for DPN treatment.
- Further research is needed to translate these findings into clinical applications.
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