ArticleOpen life sciences2019
IGF-1 Via PI3K/Akt/S6K Signaling Pathway Protects DRG Neurons with High Glucose-induced Toxicity.
Article in Open life sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- The investigational anti-B7-H3 antibody-drug conjugate vobramitamab duocarmazine exerts anti-tumor activity in vitro and in vivo in pediatric sarcoma preclinical models.Cell death & disease · 2026Article
- Stress exposure affects amyotrophic lateral sclerosis pathogenesis via PI3K/Akt and focal adhesion pathways: evidence from three experimental models.Scientific reports · 2025Article
- Exercise training benefits pancreatic islet by modulating the insulin-like growth factor 1/phosphatidylinositol 3-kinase/protein kinase B pathway.World journal of diabetes · 2025Article
- Article
- Dapagliflozin Ameliorate Type-2 Diabetes Associated Neuropathy via Regulation of IGF-1R Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Exploring the role of Prx II in mitigating endoplasmic reticulum stress and mitochondrial dysfunction in neurodegeneration.Cell communication and signaling : CCS · 2024Article
- Genetic susceptibility to high myopia in Han Chinese population.Open life sciences · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia-induced toxicity of neurons contributes to the pathogenesis and progression of diabetic neuropathy (DNP). High concentration glucose triggered reactive oxygen species (ROS) overproduction and induced cell apoptosis of neurons from dorsal root ganglion (DRG) in vitro. Currently, there is no effective therapeutic method to retard this devastating complication or neurotoxicity induced by high glucose. Insulin-like growth factor-1 (IGF-1) has multi-neurotrophic actions which need to be explored regarding its actions and mechanisms on relieving high glucose induced neurotoxicity. Herein, high concentration glucose was exposed to the DRG neurons in vitro. The effects of IGF-1 on relieving high glucose-induced neurotoxicity were evaluated. We illustrated that IGF-1 enhanced regeneration of neurites sent from DRG neuronal cell bodies and increased neuronal viability which inhibited by high glucose challenge. IGF-1 alleviated neuronal apoptosis caused by high glucose exposure. IGF-1 also suppressed the intracellular ROS overproduction and ATF3 expression upregulation which was induced by high glucose insult. The anti-neurotoxic effects of IGF-1 might be through restoration of prosurvival PI3K/Akt/S6K signaling. These data shed some light on the treatment of intractable DNP and suggested that IGF-1 might be a potential effective agent on relieving high glucose induced neurotoxicity.
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