ArticleAmerican journal of physiology. Endocrinology and metabolism2011
Inactivation of TNF-α ameliorates diabetic neuropathy in mice.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Association Between Tumor Necrosis Factor-α and Diabetic Peripheral Neuropathy in Patients with Type 2 Diabetes: a Meta-Analysis.Molecular neurobiology · 2017Pooled it
- The effect of wuling capsule on depression in Type 2 diabetic patients.Bioscience reports · 2020Trial
- Enhanced apoptosis of monocytes from complication-free juvenile-onset diabetes mellitus type 1 may be ameliorated by TNF-α inhibitors.Mediators of inflammation · 2014Trial
- Attenuation of LPS-induced inflammatory responses in J774A.1 macrophages by phenylpropanoids and ursane triterpenes from Lavandula coronopifolia Poir.Scientific reports · 2026Article
- Amelioration of gentamicin-induced acute kidney injury by trifluoperazine: in vivo mechanistic insights.Scientific reports · 2026Article
- Dietary monounsaturated fatty acids reduce nerve inflammation and improve nerve function in murine models of obesity.Frontiers in immunology · 2026Article
- Inflammatory and neurotoxic risk of atorvastatin in diabetic peripheral neuropathy: TNF-centered evidence integrating network toxicology, scRNA-Seq, and cell validation.Frontiers in chemistry · 2026Article
- Oxidative-Inflammatory Crosstalk and Multi-Target Natural Agents: Decoding Diabetic Vascular Complications.Current issues in molecular biology · 2025Review
- The Role of TNF-α in Neuropathic Pain: An Immunotherapeutic Perspective.Life (Basel, Switzerland) · 2025Review
- Dysregulated mast cell activation induced by diabetic milieu exacerbates the progression of diabetic peripheral neuropathy in mice.Nature communications · 2025Article
- The role and mechanisms of matrix metalloproteinase-9 in peripheral neuropathic pain.Frontiers in molecular neuroscience · 2025Review
- Cardiomyocyte-specific knockout of ADAM17 alleviates doxorubicin-induced cardiomyopathy via inhibiting TNFα-TRAF3-TAK1-MAPK axis.Signal transduction and targeted therapy · 2024Article
- Update on Biomarkers of Chronic Inflammatory Processes Underlying Diabetic Neuropathy.International journal of molecular sciences · 2024Review
- How inflammation dictates diabetic peripheral neuropathy: An enlightening review.CNS neuroscience & therapeutics · 2024Review
- Diabetic Neuropathy: An Overview of Molecular Pathways and Protective Mechanisms of Phytobioactives.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Effects of 1,25-Vitamin D3 and 24,25-Vitamin D3 on Corneal Nerve Regeneration in Diabetic Mice.Biomolecules · 2023Article
- Association between the Prognostic Nutritional Index and Chronic Microvascular Complications in Patients with Type 2 Diabetes Mellitus.Journal of clinical medicine · 2023Article
- Celecoxib-Loaded Cubosomal Nanoparticles as a Therapeutic Approach forMicroorganisms · 2023Article
- Effects of Topical 1,25 and 24,25 Vitamin D on Diabetic, Vitamin D Deficient and Vitamin D Receptor Knockout Mouse Corneal Wound Healing.Biomolecules · 2023Article
- Complete remission of diabetes with a transient HDAC inhibitor and insulin in streptozotocin mice.Communications biology · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor necrosis factor (TNF)-α is a potent proinflammatory cytokine involved in the pathogenesis of diabetic neuropathy. We inactivated TNF-α to determine if it is a valid therapeutic target for the treatment of diabetic neuropathy. We effected the inactivation in diabetic neuropathy using two approaches: by genetic inactivation of TNF-α (TNF-α(-/-) mice) or by neutralization of TNF-α protein using the monoclonal antibody infliximab. We induced diabetes using streptozotocin in wild-type and TNF-α(-/-) mice. We measured serum TNF-α concentration and the level of TNF-α mRNA in the dorsal root ganglion (DRG) and evaluated nerve function by a combination of motor (MNCV) and sensory (SNCV) nerve conduction velocities and tail flick test, as well as cytological analysis of intraepidermal nerve fiber density (IENFD) and immunostaining of DRG for NF-κB p65 serine-276 phosphorylated and cleaved caspase-3. Compared with nondiabetic mice, TNF-α(+/+) diabetic mice displayed significant impairments of MNCV, SNCV, tail flick test, and IENFD as well as increased expression of NF-κB p65 and cleaved caspase-3 in their DRG. In contrast, although nondiabetic TNF-α(-/-) mice showed mild abnormalities of IENFD under basal conditions, diabetic TNF-α(-/-) mice showed no evidence of abnormal nerve function tests compared with nondiabetic mice. A single injection of infliximab in diabetic TNF-α(+/+) mice led to suppression of the increased serum TNF-α and amelioration of the electrophysiological and biochemical deficits for at least 4 wk. Moreover, the increased TNF-α mRNA expression in diabetic DRG was also attenuated by infliximab, suggesting infliximab's effects may involve the local suppression of TNF-α. Infliximab, an agent currently in clinical use, is effective in targeting TNF-α action and expression and amelioration of diabetic neuropathy in mice.
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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.