ArticleCell death & disease2014
D-ribosylation induces cognitive impairment through RAGE-dependent astrocytic inflammation.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose.Frontiers in aging neuroscience · 2022Pooled it
- Interacting proteins of AMPK studied using TurboID proximity labeling technology.Experimental and therapeutic medicine · 2026Article
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling.Acta biochimica et biophysica Sinica · 2025Article
- D-ribose metabolic disorder and diabetes mellitus.Molecular biology reports · 2024Review
- The role of neurovascular coupling dysfunction in cognitive decline of diabetes patients.Frontiers in neuroscience · 2024Review
- Flavonols as a Potential Pharmacological Intervention for Alleviating Cognitive Decline in Diabetes: Evidence from Preclinical Studies.Life (Basel, Switzerland) · 2023Review
- Severe Obesity in Women Can Lead to Worse Memory Function and Iron Dyshomeostasis Compared to Lower Grade Obesity.International journal of endocrinology · 2023Article
- Ribose Intake as Food Integrator: Is It a Really Convenient Practice?Biomolecules · 2022Review
- Protein Modification with Ribose GeneratesInternational journal of molecular sciences · 2022Article
- D-ribose: Potential clinical applications in congestive heart failure and diabetes, and its complications (Review).Experimental and therapeutic medicine · 2021Review
- Chronic D-ribose and D-mannose overload induce depressive/anxiety-like behavior and spatial memory impairment in mice.Translational psychiatry · 2021Article
- Glycated albumin precipitation using aptamer conjugated magnetic nanoparticles.Scientific reports · 2020Article
- D-ribose and pathogenesis of Alzheimer's disease.Molecular biology reports · 2020Review
- D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy.Aging · 2019Article
- [Serum metabolomics of preterm and full-term infants based on gas chromatography-mass spectrometry].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
- D-Ribose Induces Podocyte NLRP3 Inflammasome Activation and Glomerular Injury via AGEs/RAGE Pathway.Frontiers in cell and developmental biology · 2019Article
- Protective Effects of Kaempferol on D-Ribose-Induced Mesangial Cell Injury.Oxidative medicine and cellular longevity · 2019Article
- High glucose-induced complement component 3 up-regulation via RAGE-p38MAPK-NF-κB signalling in astrocytes: In vivo and in vitro studies.Journal of cellular and molecular medicine · 2018Article
- D-ribose induces nephropathy through RAGE-dependent NF-κB inflammation.Archives of pharmacal research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-enzymatic glycation of proteins by reducing saccharides for instance D-glucose is an important post-translational modification regulating protein function. Already two centuries ago, D-glucose (Glc) was identified in the urine of diabetic patients. Recently, abnormally high level of D-ribose (Rib) in the urine of type 2 diabetics has been discovered, which is highly active in protein glycation, resulting in the production of advanced glycation end products (AGEs). Accumulation of AGEs leads to altered cellular function, for example AGE accumulation in the nervous system impairs cognitive ability, yet the mechanisms mediating this process for Rib are unknown. Here we found that treatment with Rib accelerated AGE formation in U251 and U87MG astrocytoma cells and in mouse brain, inducing upregulation of receptor for AGEs (RAGE). Astrocytoma cells with elevated levels of RAGE displayed enhanced activity of the proinflammatory nuclear transcription factor kappaB and increased expression of tumor necrosis factor alpha and glial fibrillary acidic protein. Moreover, injection of Rib induced astrocyte activation in mouse hippocampus and impaired spatial learning and memory abilities. These results indicate that mouse spatial cognitive impairment caused by Rib-derived AGEs is correlated with activation of an astrocyte-mediated, RAGE-dependent inflammatory response. This study may provide insights into the mechanism of Rib-involved cognitive impairments and diabetic encephalopathy.
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