ReviewAmino acids2012
Advanced glycation endproducts: from precursors to RAGE: round and round we go.
Review in Amino acids, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 152 citations in OpenAlex.
- Lifestyle Modification: Evaluation of the Effects of Physical Activity and Low-Glycemic-Index Mediterranean Diet on Fibrosis Score.Nutrients · 2023Trial
- Dysfunctional protection against advanced glycation due to thiamine metabolism abnormalities in gestational diabetes.Glycoconjugate journal · 2016Trial
- Advanced glycation end products and the CALLY index reflect inflammatory burden in familial Mediterranean fever.Scientific reports · 2026Article
- Effect of Melatonin as an Adjunct to NSPT on Periodontal and Systemic Outcomes in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of RCTs.Journal of clinical medicine · 2026Review
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- Molecular frontiers in hemodialysis: unraveling the role of membranes in gene expression, epigenetics, and inflammatory pathways.International urology and nephrology · 2025Review
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- Unveiling the depths of pelvic organ prolapse: From risk factors to therapeutic methods (Review).Experimental and therapeutic medicine · 2025Review
- Molecular Basis for the Involvement of Mammalian Serum Albumin in the AGE/RAGE Axis: A Comprehensive Computational Study.International journal of molecular sciences · 2024Article
- Pharmacological Action of Baicalin on Gestational Diabetes Mellitus in Pregnant Animals Induced by Streptozotocin via AGE-RAGE Signaling Pathway.Applied biochemistry and biotechnology · 2024Article
- Article
- Potential Metabolic Pathways Involved in Osteoporosis and Evaluation of Fracture Risk in Individuals with Diabetes.BioMed research international · 2024Review
- Effect of β-amyloid on blood-brain barrier properties and function.Biophysical reviews · 2023Review
- Blocking RAGE expression after injury reduces inflammation in mouse model of acute lung injury.Respiratory research · 2023Article
- The Role of Advanced Glycation End Products on Dyslipidemia.Metabolites · 2023Review
- Potential novel markers in IBD and CRC diagnostics. Are MMP-19 and RAGE promising candidates?Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2022Article
- Docking and Molecular Dynamics-Based Identification of Interaction between Various Beta-Amyloid Isoforms and RAGE Receptor.International journal of molecular sciences · 2022Article
- The role of oxidative stress in ovarian aging: a review.Journal of ovarian research · 2022Review
- The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice.International journal of molecular sciences · 2022Article
- The mFrontiers in endocrinology · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The formation of advanced glycation endproducts (AGEs) occurs in diverse settings such as diabetes, aging, renal failure, inflammation and hypoxia. The chief cellular receptor for AGEs, RAGE, transduces the effects of AGEs via signal transduction, at least in part via processes requiring the RAGE cytoplasmic domain binding partner, diaphanous-1 or mDia1. Data suggest that RAGE perpetuates the inflammatory signals initiated by AGEs via multiple mechanisms. AGE-RAGE interaction stimulates generation of reactive oxygen species and inflammation--mechanisms which enhance AGE formation. Further, recent data in type 1 diabetic kidney reveal that deletion of RAGE prevents methylglyoxal accumulation, at least in part via RAGE-dependent regulation of glyoxalase-1, a major enzyme involved in methylglyoxal detoxification. Taken together, these considerations place RAGE in the center of biochemical and molecular stresses that characterize the complications of diabetes and chronic disease. Stopping RAGE-dependent signaling may hold the key to interrupting cycles of cellular perturbation and tissue damage in these disorders.
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Identifiers
What OpenQuestion holds
Registered trials
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.