ArticleNeurochemical research2002
Hyperglycemia triggers abnormal signaling and proliferative responses in Schwann cells.
Article in Neurochemical research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Models of hyperglycaemia in diabetes mellitus and its complications.Nature reviews. Endocrinology · 2026Review
- Crumbling Pathogenesis and Biomarkers for Diabetic Peripheral Neuropathy.Biomedicines · 2025Review
- Novel strategy: Identifying new markers for demyelination in diabetic distal symmetrical polyneuropathy.Heliyon · 2024Article
- Insulin enhances neurite extension and myelination of diabetic neuropathy neurons.The Korean journal of pain · 2022Article
- Taurine reduces nitrosative stress and nitric oxide synthase expression in high glucose-exposed human Schwann cells.Experimental neurology · 2012Article
- Sensory neurons and schwann cells respond to oxidative stress by increasing antioxidant defense mechanisms.Antioxidants & redox signaling · 2009Article
- Effect of Jinmaitong serum on the proliferation of rat Schwann cells cultured in high glucose medium.Chinese journal of integrative medicine · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Peripheral neuropathy is a serious diabetic complication. Delayed nerve regeneration in diabetic animal models suggests abnormalities in proliferation/differentiation of Schwann cells (SC). We recently reported that endothelins (ETs) regulate proliferation and phenotype in primary and immortalized SC (iSC). We now investigated changes in the effects of ETs on SC proliferation and signaling in nerve segments from streptozotocin-induced diabetic rats and in iSC exposed to high glucose. Cultured explants from diabetic rats displayed a delay in the time-course of [3H]-thymidine incorporation as well as enhanced sensitivity to endothelin-1 (ET-1) or insulin. iSC cultured in high (25 mM) glucose-containing media also exhibited higher [3H]-thymidine incorporation, along with an enhanced activation of p38 mitogen-activated protein kinase and phospholipase C in response to ET-1 or platelet-derived growth factor as compared to controls (5.5 mM glucose). These studies support an extra-vascular role of ETs in peripheral nerves and SC. The increased sensitivity to ET-1 in nerves and iSC exposed to high glucose may contribute to abnormal SC proliferation characterizing diabetic neuropathy.
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What Socratic holds
Registered trials
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.