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September 19, 2025Diabetic Medicine

Advanced glycation end products mediated diabetic neuropathic pain via activation protein tyrosine phosphatase 1B in the spinal cord dorsal horn

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Increased plasma AGEs elevated hyperalgesia in diabetes, while PTP1B knockout significantly alleviated this response.
Electrophysiological recordings demonstrated enhanced NMDAR activity due to AGEs, which was inhibited by PTP1B knockdown.
Biochemical analysis revealed altered phosphorylation states of Src and NMDAR in response to AGEs, influenced by PTP1B.
This study proposes targeting the AGEs-PTP1B-NMDAR pathway as a novel therapeutic strategy for managing diabetic neuropathic pain.

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Investigation reveals how elevated AGEs trigger hyperalgesia via PTP1B in spinal cord models, suggesting new treatment avenues.

Wang et al. (2025) studied this question.

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