ArticleBMC neuroscience2020
NGF receptors and PI3K/AKT pathway involved in glucose fluctuation-induced damage to neurons and α-lipoic acid treatment.
Article in BMC neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Reduced nerve growth factor (NGF) mediates arsenic-induced mitochondrial dynamics imbalance and neuronal damage both in vivo and in vitro.Journal of Zhejiang University. Science. B · 2026Article
- The Interaction Between Insulin Resistance and Neuroinflammation in the Brain and Its Impact on Diabetic Encephalopathy.Biology · 2026Review
- Low-Level Light Therapy in Postherpetic Neuralgia: A Review of Mechanistic Insights and Clinical Implications.Cellular and molecular neurobiology · 2026Review
- Modulatory Role of Arbutin on Hepatic Inflammation and Apoptosis After Mild Repetitive Traumatic Brain Injury in Experimental Rats: Involvement of NGF/TrkA and IL-6/JAK2/STAT3 Immune Signaling Crosstalk.Biochemistry research international · 2026Article
- Optimization and characterization of acute radiation-induced esophagitis in mice.Radiation oncology (London, England) · 2025Article
- Mechanisms of Variation in Abdominal Adipose Color Among Male Kazakh Horses Through Non-Coding RNA Sequencing.Biology · 2025Article
- From neuromodulation to bone homeostasis: therapeutic targets of nerve growth factor in skeletal diseases.Frontiers in pharmacology · 2025Review
- Article
- Predictive Value of Combined HbA1c and Neutrophil-to-Lymphocyte Ratio for Diabetic Peripheral Neuropathy in Type 2 Diabetes.Medical science monitor : international medical journal of experimental and clinical research · 2024Observational
- Enhancement of neural regeneration as a therapeutic strategy for Alzheimer's disease (Review).Experimental and therapeutic medicine · 2023Review
- Detection and Quantification of Neurotrophin-3 (NT-3) and Nerve Growth Factor (NGF) Levels in Early Second Trimester Amniotic Fluid: Investigation into a Possible Correlation with Abnormal Fetal Growth Velocity Patterns.Journal of clinical medicine · 2023Article
- Older postmenopausal women with lower lean mass have hypermethylated sites in the PI3K-Akt pathway.Frontiers in physiology · 2023Article
- Nerve growth factor promotes differentiation and protects the oligodendrocyte precursor cells fromFrontiers in neuroscience · 2023Article
- Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention.Revista brasileira de farmacognosia : orgao oficial da Sociedade Brasileira de Farmacognosia · 2023Review
- SorCS3 promotes the internalization of p75Cell death & disease · 2022Article
- Effects of regenerative peripheral nerve interface on dorsal root ganglia neurons following peripheral axotomy.Frontiers in neuroscience · 2022Article
- Glucose Variability: How Does It Work?International journal of molecular sciences · 2021Review
- Neurotrophins as Key Regulators of Cell Metabolism: Implications for Cholesterol Homeostasis.International journal of molecular sciences · 2021Review
- LianXia Formula Granule Attenuates Cardiac Sympathetic Remodeling in Rats with Myocardial Infarction via the NGF/TrKA/PI3K/AKT Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlucose fluctuation promotes neuronal apoptosis, which plays a central role in diabetic encephalopathy (DE). Nerve growth factor (NGF), and its interaction with high-affinity (TrkA) and low-affinity (p75NTR) receptors, are involved in neuronal survival. NGF/TrkA contributes to the activation of the PI3K/AKT pathway, which is beneficial for neuronal survival, and α-Lipoic acid (ALA) exerts clinically favorable neuroprotective effects in the periphery. Whether NGF receptors and the PI3K/AKT pathway are involved in glucose fluctuation-induced neuronal damage, as well as the potential molecular mechanism of ALA in protecting glucose fluctuation-induced neuronal damage, remain unclear.
resultsThe results indicated that constant high glucose (CHG) and intermittent high glucose (IHG) significantly increased the expression of Bax and caspase-3, and decreased the expression of TrkA/p75NTR and p-AKT/AKT, while ALA stimulation reversed the above proteins in PC12 cells. IHG stimulates apoptosis more effectively than CHG in PC12 cells, which is related to the PI3K/AKT pathway but not to the TrkA/p75NTR. Furthermore, neuronal apoptosis induced by IHG was aggravated by the TrkA inhibitor K252a or the PI3K/AKT inhibitor LY294002, but this effect was alleviated by the p75NTR inhibitor TAT-pep5.
conclusionGlucose fluctuation induced cell apoptosis by regulating the TrkA/p75NTR and PI3K/AKT pathway, meanwhile ALA exhibited neuroprotective effects in response to IHG and CHG. These observations indicated that the PI3K/AKT pathway and the balance of TrkA/p75NTR are likely to serve as potential therapeutic targets for DE. In addition, ALA could be a possible therapeutic drug for DE.
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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.