ArticleCellular and molecular life sciences : CMLS2022
CEBPβ regulation of endogenous IGF-1 in adult sensory neurons can be mobilized to overcome diabetes-induced deficits in bioenergetics and axonal outgrowth.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- A bioactivity-enhanced thermosensitive amnion-derived hydrogel with sustained IGF-1 release: A multitargeted and efficient strategy for corneal injury repair.Bioactive materials · 2027Article
- Contemporary Strategies of Gene and Cell Therapy in the Treatment of Peripheral Nervous System Injuries and Disorders.International journal of molecular sciences · 2026Review
- Diabetes and its complications: molecular mechanisms, prevention and treatment.Signal transduction and targeted therapy · 2026Review
- Deficiency of Aging-Related Gene Chitinase-Like 4 Impairs Olfactory Epithelium Homeostasis.Cell proliferation · 2025Article
- Advances in research on mitochondrial dysfunction in neurodegenerative diseases.Journal of neurology · 2025Review
- Role of Mitochondrial Dysfunction in Neuropathy.International journal of molecular sciences · 2025Review
- Maternal behavior promotes resilience to adolescent stress in mice through a microglia-neuron axis.Nature communications · 2025Article
- Eye on the horizon: The metabolic landscape of the RPE in aging and disease.Progress in retinal and eye research · 2025Review
- Roles of C/EBPβ/AEP in Neurodegenerative Diseases.Current topics in medicinal chemistry · 2025Review
- Diminished levels of insulin-like growth factor-1 may be a risk factor for peripheral neuropathy in type 2 diabetes patients.Journal of diabetes investigation · 2024Article
- The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing.Translational neurodegeneration · 2024Review
- Neuronal glycolysis: focus on developmental morphogenesis and localized subcellular functions.Communicative & integrative biology · 2024Review
- CEBP-β and PLK1 as Potential Mediators of the Breast Cancer/Obesity Crosstalk: In Vitro and In Silico Analyses.Nutrients · 2023Article
- Transcriptional Profiling of Rat Prefrontal Cortex after Acute Inescapable Footshock Stress.Genes · 2023Article
- Identification of the molecular mechanism of insulin-like growth factor-1 (IGF-1): a promising therapeutic target for neurodegenerative diseases associated with metabolic syndrome.Cell & bioscience · 2023Review
- C/EBPβ Regulates TFAM Expression, Mitochondrial Function and Autophagy in Cellular Models of Parkinson's Disease.International journal of molecular sciences · 2023Article
- IGF/IGF-1R signal pathway in pain: a promising therapeutic target.International journal of biological sciences · 2023Review
- Pathogenesis of Dementia.International journal of molecular sciences · 2022Review
- Roles of traditional chinese medicine regulating neuroendocrinology on AD treatment.Frontiers in endocrinology · 2022Review
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Aberrant insulin-like growth factor 1 (IGF-1) signaling has been proposed as a contributing factor to the development of neurodegenerative disorders including diabetic neuropathy, and delivery of exogenous IGF-1 has been explored as a treatment for Alzheimer's disease and amyotrophic lateral sclerosis. However, the role of autocrine/paracrine IGF-1 in neuroprotection has not been well established. We therefore used in vitro cell culture systems and animal models of diabetic neuropathy to characterize endogenous IGF-1 in sensory neurons and determine the factors regulating IGF-1 expression and/or affecting neuronal health. Single-cell RNA sequencing (scRNA-Seq) and in situ hybridization analyses revealed high expression of endogenous IGF-1 in non-peptidergic neurons and satellite glial cells (SGCs) of dorsal root ganglia (DRG). Brain cortex and DRG had higher IGF-1 gene expression than sciatic nerve. Bidirectional transport of IGF-1 along sensory nerves was observed. Despite no difference in IGF-1 receptor levels, IGF-1 gene expression was significantly (P < 0.05) reduced in liver and DRG from streptozotocin (STZ)-induced type 1 diabetic rats, Zucker diabetic fatty (ZDF) rats, mice on a high-fat/ high-sugar diet and db/db type 2 diabetic mice. Hyperglycemia suppressed IGF-1 gene expression in cultured DRG neurons and this was reversed by exogenous IGF-1 or the aldose reductase inhibitor sorbinil. Transcription factors, such as NFAT1 and CEBPβ, were also less enriched at the IGF-1 promoter in DRG from diabetic rats vs control rats. CEBPβ overexpression promoted neurite outgrowth and mitochondrial respiration, both of which were blunted by knocking down or blocking IGF-1. Suppression of endogenous IGF-1 in diabetes may contribute to neuropathy and its upregulation at the transcriptional level by CEBPβ can be a promising therapeutic approach.
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