ArticleDiabetes2013
RAGE deficiency improves postinjury sciatic nerve regeneration in type 1 diabetic mice.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 87 citations in OpenAlex.
- Modeling Diabetic Neuropathy: Injury Biomarkers for Early Detection Through Neuronal and Glial In Vitro Models.International journal of molecular sciences · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Immunological mechanisms and therapeutic advances in diabetic neuropathy.Journal of neurology · 2026Review
- The Effect of RAGE-Diaph1 Signaling Inhibition on the Progression of Peripheral Neuropathy in Diabetic Mice.International journal of molecular sciences · 2025Article
- RAGE Cytosolic Partner Diaph1 Does Not Play an Essential Role in Diabetic Peripheral Neuropathy Progression.Cells · 2025Article
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- Lactoferrin-derived peptide PXL01 impacts nerve regeneration after sciatic nerve reconstruction in healthy and diabetic rats.Frontiers in cell and developmental biology · 2025Article
- Novel insights into neuropathy: The impact of prolonged hyperglycemia on long non-coding RNA expression.PloS one · 2025Article
- Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing.Frontiers in medicine · 2025Review
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Review
- The contribution of adiponectin to diabetic retinopathy progression: Association with the AGEs-RAGE pathway.Heliyon · 2024Article
- Pathological evaluation of the pathogenesis of diabetes mellitus and diabetic peripheral neuropathy.Pathology international · 2024Review
- Glycation resistance and life-history traits: lessons from non-conventional animal models.Biology letters · 2024Review
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- Combination therapy is it in the future for successfully treating peripheral diabetic neuropathy?Frontiers in endocrinology · 2024Review
- Association between the Prognostic Nutritional Index and Chronic Microvascular Complications in Patients with Type 2 Diabetes Mellitus.Journal of clinical medicine · 2023Article
- Novel insights into the nervous system affected by prolonged hyperglycemia.Journal of molecular medicine (Berlin, Germany) · 2023Article
- RAGE activation in macrophages and development of experimental diabetic polyneuropathy.JCI insight · 2022Article
- Role of RAGE in the Pathogenesis of Neurological Disorders.Neuroscience bulletin · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Peripheral neuropathy and insensate limbs and digits cause significant morbidity in diabetic individuals. Previous studies showed that deletion of the receptor for advanced end-glycation products (RAGE) in mice was protective in long-term diabetic neuropathy. Here, we tested the hypothesis that RAGE suppresses effective axonal regeneration in superimposed acute peripheral nerve injury attributable to tissue-damaging inflammatory responses. We report that deletion of RAGE, particularly in diabetic mice, resulted in significantly higher myelinated fiber densities and conduction velocities consequent to acute sciatic nerve crush compared with wild-type control animals. Consistent with key roles for RAGE-dependent inflammation, reconstitution of diabetic wild-type mice with RAGE-null versus wild-type bone marrow resulted in significantly improved axonal regeneration and restoration of function. Diabetic RAGE-null mice displayed higher numbers of invading macrophages in the nerve segments postcrush compared with wild-type animals, and these macrophages in diabetic RAGE-null mice displayed greater M2 polarization. In vitro, treatment of wild-type bone marrow-derived macrophages with advanced glycation end products (AGEs), which accumulate in diabetic nerve tissue, increased M1 and decreased M2 gene expression in a RAGE-dependent manner. Blockade of RAGE may be beneficial in the acute complications of diabetic neuropathy, at least in part, via upregulation of regeneration signals.
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What OpenQuestion 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 OpenQuestion graph.