ArticleDiabetes2008
RAGE and modulation of ischemic injury in the diabetic myocardium.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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
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Who cites it
56 citing papers in PubMed, 109 citations in OpenAlex.
- Rescuing anxiety by targeting the neuronal-astrocytic iron signaling axis in male mice.Signal transduction and targeted therapy · 2026Article
- Clinical Significance of Cardio-Ankle Vascular Index in Stage A/B Heart Failure Patients With Type 2 Diabetes Mellitus.Journal of clinical medicine research · 2026Article
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- RAGE signaling in acute myocardial infarction: sRAGE as a dynamic biomarker and emerging therapeutic target.Frontiers in endocrinology · 2026Review
- Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- Assessment of cardiac and skeletal muscle metabolites usingNMR in biomedicine · 2025Article
- Review
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors.Life (Basel, Switzerland) · 2023Review
- The RAGE/DIAPH1 Signaling Axis & Implications for the Pathogenesis of Diabetic Complications.International journal of molecular sciences · 2022Review
- Small-molecule antagonism of the interaction of the RAGE cytoplasmic domain with DIAPH1 reduces diabetic complications in mice.Science translational medicine · 2021Article
- Diabetes and Cardiovascular Complications: The Epidemics Continue.Current cardiology reports · 2021Review
- Journey to a Receptor for Advanced Glycation End Products Connection in Severe Acute Respiratory Syndrome Coronavirus 2 Infection: With Stops Along the Way in the Lung, Heart, Blood Vessels, and Adipose Tissue.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Skin Autofluorescence as a Predictor of First Heart Failure Hospitalization in Patients With Heart Failure With Preserved Ejection Fraction.Cardiology research · 2020Article
- Role of DJ-1 in Modulating Glycative Stress in Heart Failure.Journal of the American Heart Association · 2020Article
- Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models.Frontiers in cardiovascular medicine · 2020Review
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- Clinical Significance of Skin Autofluorescence in Elderly Patients With Long-Standing Persistent Atrial Fibrillation.Cardiology research · 2019Article
- Diabetes Mellitus and Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- RNA Expression Profile and Alternative Splicing Signatures of Genistein-Treated Breeder Hens Revealed by Hepatic Transcriptomic Analysis.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveSubjects with diabetes experience an increased risk of myocardial infarction and cardiac failure compared with nondiabetic age-matched individuals. The receptor for advanced glycation end products (RAGE) is upregulated in diabetic tissues. In this study, we tested the hypothesis that RAGE affected ischemia/reperfusion (I/R) injury in the diabetic myocardium. In diabetic rat hearts, expression of RAGE and its ligands was enhanced and localized particularly to both endothelial cells and mononuclear phagocytes. RESEARCH DESIGN AND
methodsTo specifically dissect the impact of RAGE, homozygous RAGE-null mice and transgenic (Tg) mice expressing cytoplasmic domain-deleted RAGE (DN RAGE), in which RAGE-dependent signal transduction was deficient in endothelial cells or mononuclear phagocytes, were rendered diabetic with streptozotocin. Isolated perfused hearts were subjected to I/R.
resultsDiabetic RAGE-null mice were significantly protected from the adverse impact of I/R injury in the heart, as indicated by decreased release of LDH and lower glycoxidation products carboxymethyl-lysine (CML) and pentosidine, improved functional recovery, and increased ATP. In diabetic Tg mice expressing DN RAGE in endothelial cells or mononuclear phagocytes, markers of ischemic injury and CML were significantly reduced, and levels of ATP were increased in heart tissue compared with littermate diabetic controls. Furthermore, key markers of apoptosis, caspase-3 activity and cytochrome c release, were reduced in the hearts of diabetic RAGE-modified mice compared with wild-type diabetic littermates in I/R.
conclusionsThese findings demonstrate novel and key roles for RAGE in I/R injury in the diabetic heart.
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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.