ArticleACS pharmacology & translational science2025
Schwann Cell Protein Kinase RNA-like ER Kinase (PERK) Is Not Necessary for the Development of Diabetic Peripheral Neuropathy but Negates the Efficacy of Cemdomespib Therapy.
Article in ACS pharmacology & translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Targeting endoplasmic reticulum stress: a novel therapeutic strategy for neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
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Authors and funding
2 authors.
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Abstract
Diabetic peripheral neuropathy (DPN) is a common complication of diabetes arising in part from glycemic damage to neurons and Schwann cells (SC). While the pathogenic mechanisms of DPN are complex, mitochondrial dysfunction and endoplasmic reticulum (ER) stress contribute to the development of DPN and serve as therapeutic targets for disease modification. Cemdomespib is an orally bioavailable small molecule which alleviates clinical indices of DPN that correlate with improvements in neuronal oxidative stress and mitochondrial bioenergetics. However, the contribution of SC ER stress in the onset of DPN and the therapeutic efficacy of cemdomespib remains unknown. To address this issue, mice expressing a conditional deletion of protein kinase RNA-like ER kinase (PERK) in myelinating SCs (SC-cPERK KO) and control SC-PERK
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