ReviewFrontiers in endocrinology2026
Mechanisms, translational opportunities for diabetic polyneuropathy.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Diabetic polyneuropathy (DPN) is a common complication of types 1 and 2 diabetes mellitus (DM). Peripheral sensory axons are early and primary targets of DPN, rendering sensory loss, pain and impaired quality of life. While several metabolic and other abnormalities, including abnormal insulin signaling and mitochondrial dysfunction contribute toward DPN, effective therapy to reverse or arrest the disorder is not currently available. DPN is a degenerative condition that involves retraction of distal sensory terminals and failure of regenerative repair. This review summarizes current mechanisms of DPN and potential new approaches that may offer translational opportunities for treatment. Many of these targets have yet to be explored in multiple DM models/paradigms and have not yet entered clinical trials. Nonetheless, specific regeneration pathways may offer a future role to encourage sensory axon resilience and regrowth.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.