ArticleDiabetes2025
Exploring Structural and Molecular Features of Sciatic Nerve Lesions in Diabetic Neuropathy: Unveiling Pathogenic Pathways and Targets.
Article in Diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Who cites it
5 citing papers in PubMed.
- Leaving no stone unturned from bench to bedside: Challenges and future perspectives in diabetic polyneuropathy.Journal of diabetes investigation · 2026Article
- Noninvasive MRI biomarkers in diabetic neuropathy: correlation with electrophysiology, clinical scores, and nerve pathology.Neuroradiology · 2026Review
- Review
- Diabetic neuropathy's immune-metabolic network: mechanistic complexity, therapeutic challenges, and the path forward.Frontiers in immunology · 2026Review
- Diagnostic value of shear wave elastography for diabetic peripheral neuropathy: comparison between junior radiologists and senior radiologists.BMC medical imaging · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Lesioned fascicles (LFs) in the sciatic nerves of individuals with diabetic neuropathy (DN) correlate with clinical symptom severity. This study aimed to characterize the structural and molecular composition of these lesions to better understand DN pathogenesis. Sciatic nerves from amputees with and without type 2 diabetes (T2D) were examined using ex vivo magnetic resonance neurography, in vitro imaging, and proteomic analysis. Lesions were only found in T2D donors and exhibited significant structural abnormalities, including axonal degeneration, demyelination, and impaired blood-nerve barrier (BNB). Although non-LFs from T2D donors showed activation of neuroprotective pathways, LFs lacked this response and instead displayed increased complement activation via the classical pathway. The detection of liver-derived acute-phase proteins suggests that BNB disruption facilitates harmful interorgan communication between the liver and nerves. These findings reveal key molecular mechanisms contributing to DN and highlight potential targets for therapeutic intervention. ARTICLE HIGHLIGHTS:
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