ArticleMolecular brain2022
High glucose and palmitic acid induces neuronal senescence by NRSF/REST elevation and the subsequent mTOR-related autophagy suppression.
Article in Molecular brain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- HMGB1 aggravates neuronal ferroptosis and microglial inflammation in metabolic syndrome-associated cognitive impairment via the NRF2-autophagic flux axis.Molecular biomedicine · 2026Article
- The role of lipid metabolism in neuronal senescence.FEBS open bio · 2026Review
- Anti-cancer effect of palmitic acid against the endometrial cancer progression via inducing ferroptosis.Biochemistry and biophysics reports · 2026Article
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells.Research (Washington, D.C.) · 2026Article
- Regulation of nuclear transport of the transcriptional factor REST improves axon regeneration in peripheral nerves.Molecular medicine reports · 2025Article
- Alleviated Neuroinflammation and Increased Neuritogenesis by Palmitic Acid from Cissus quadrangularis.Molecular neurobiology · 2025Article
- The multifaceted role of KIF15 in cancer progression and therapy.Investigational new drugs · 2025Review
- The secretome of senescent monocytes predicts age-related clinical outcomes in humans.Nature aging · 2025Article
- Cholesterol's hidden impact: the nonlinear link between remnant cholesterol (RC) and phenotypic age acceleration (PhenoAgeAccel).Biogerontology · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Upregulation of SQSTM1 Regulates Ferroptosis and Oxidative Stress in Müller Cells of the Diabetic Neural Retina by Modulating ACSL4.Journal of diabetes research · 2025Article
- ER-α36 prevents high glucose-induced cellular senescence and apoptosis in renal tubular cell.Frontiers in endocrinology · 2025Article
- Syringin protects high glucose-induced BMSC injury, cell senescence, and osteoporosis by inhibiting JAK2/STAT3 signaling.Journal of applied biomedicine · 2024Article
- Article
- REST-dependent downregulation of von Hippel-Lindau tumor suppressor promotes autophagy in SHH-medulloblastoma.Scientific reports · 2024Article
- KIF15 promotes human glioblastoma progression under the synergistic transactivation of REST and P300.International journal of biological sciences · 2024Article
- Autophagy and the pancreas: Healthy and disease states.Frontiers in cell and developmental biology · 2024Review
- Autophagy Regulates Ferroptosis-Mediated Diabetic Liver Injury by Modulating the Degradation of ACSL4.Journal of diabetes research · 2024Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell senescence is a basic aging mechanism. Previous studies have found that the cellular senescence in adipose tissue and other tissues, such as the pancreas, muscle and liver, is associated with the pathogenesis and progression of type 2 diabetes; however, strong evidence of whether diabetes directly causes neuronal senescence in the brain is still lacking. In this study, we constructed a high glucose and palmitic acid (HGP) environment on PC12 neuronal cells and primary mouse cortical neurons to simulate diabetes. Our results showed that after HGP exposure, neurons exhibited obvious senescence-like phenotypes, including increased NRSF/REST level, mTOR activation and cell autophagy suppression. Downregulation of NRSF/REST could remarkably alleviate p16, p21 and γH2A.X upregulations induced by HGP treatment, and enhance mTOR-autophagy of neurons. Our results suggested that the diabetic condition could directly induce neuronal senescence, which is mediated by the upregulation of NRSF/REST and subsequent reduction of mTOR-autophagy.
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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.