ReviewFrontiers in cardiovascular medicine2020
Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models.
Review in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 3 of them syntheses that pooled it.
What it found
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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.
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Who cites it
104 citing papers in PubMed, 3 syntheses or guidelines pooled it, 211 citations in OpenAlex.
- Soluble receptor for advanced glycation end products (sRAGE) is associated with obesity rates: a systematic review and meta-analysis of cross-sectional study.BMC endocrine disorders · 2023Pooled it
- Circulating Advanced Glycation End Products and Their Soluble Receptors in Relation to All-Cause and Cardiovascular Mortality: A Systematic Review and Meta-analysis of Prospective Observational Studies.Advances in nutrition (Bethesda, Md.) · 2021Pooled it
- Novel inflammatory biomarkers in the prognosis of COVID-19.Therapeutic advances in respiratory diseasePooled it
- Therapeutic impact of vildagliptin vs. gliclazide on insulin resistance and advanced glycated end product levels in newly diagnosed Egyptian diabetics: a randomized controlled trial.European journal of clinical pharmacology · 2025Trial
- Genetic and pharmacologic modulation of RAGE rescues the diabetes-mediated impairments to bone at multiple length scales.bioRxiv : the preprint server for biology · 2026Article
- The AGE-RAGE Pathway in Endometriosis: A Focused Mechanistic Review and Structured Evidence Map.International journal of molecular sciences · 2026Review
- Adiponectin deficiency drives cerebrovascular dysfunction and synergizes with amyloid-β to exacerbate alzheimer's pathology.Alzheimer's research & therapy · 2026Article
- Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026Review
- The Perspective of Using Ischemic Tolerance in Clinical Practice.Biomedicines · 2026Review
- Advanced glycation end products and RAGE signaling in diabetic cardiomyopathy: distinct mechanisms, human evidence, and translational barriers.Frontiers in cardiovascular medicine · 2026Review
- AldehydeFrontiers in medicine · 2026Article
- Recent Advances in the Study of Diabetic Cardiac Autonomic Neuropathy.Reviews in cardiovascular medicine · 2026Review
- Development of New Benzo[b]Thiophene-2-Carboxamide Derivatives as Advanced Glycation End-Products Receptor (RAGE) Antagonists.ChemMedChem · 2026Article
- HDL metabolism and function in diabetes mellitus.Nature reviews. Endocrinology · 2026Review
- Advanced glycation end products (AGEs) and their role in diabetes mellitus and related complications: mechanisms and therapeutic insights.Glycoconjugate journal · 2025Review
- The Effect of RAGE-Diaph1 Signaling Inhibition on the Progression of Peripheral Neuropathy in Diabetic Mice.International journal of molecular sciences · 2025Article
- RAGE Cytosolic Partner Diaph1 Does Not Play an Essential Role in Diabetic Peripheral Neuropathy Progression.Cells · 2025Article
- Human iPSC-derived salivary gland organoids model diabetic salivary gland dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial dynamics in diabetic peripheral neuropathy: Pathogenesis, progression, and therapeutic approaches.Medicine · 2025Review
- Soluble Receptor of Advanced Glycation End Products and Cardiometabolic Markers in Children.Cureus · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity and diabetes are leading causes of cardiovascular morbidity and mortality. Although extensive strides have been made in the treatments for non-diabetic atherosclerosis and its complications, for patients with diabetes, these therapies provide less benefit for protection from cardiovascular disease (CVD). These considerations spur the concept that diabetes-specific, disease-modifying therapies are essential to identify, especially as the epidemics of obesity and diabetes continue to expand. Hence, as hyperglycemia is a defining feature of diabetes, it is logical to probe the impact of the specific consequences of hyperglycemia on the vessel wall, immune cell perturbation, and endothelial dysfunction-all harbingers to the development of CVD. In this context, high levels of blood glucose stimulate the formation of the irreversible advanced glycation end products, the products of non-enzymatic glycation and oxidation of proteins and lipids. AGEs accumulate in diabetic circulation and tissues and the interaction of AGEs with their chief cellular receptor, receptor for AGE or RAGE, contributes to vascular and immune cell perturbation. The cytoplasmic domain of RAGE lacks endogenous kinase activity; the discovery that this intracellular domain of RAGE binds to the formin, DIAPH1, and that DIAPH1 is essential for RAGE ligand-mediated signal transduction, identifies the specific cellular means by which RAGE functions and highlights a new target for therapeutic interruption of RAGE signaling. In human subjects, prominent signals for RAGE activity include the presence and levels of two forms of soluble RAGE, sRAGE, and endogenous secretory (es) RAGE. Further, genetic studies have revealed single nucleotide polymorphisms (SNPs) of the
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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.