ArticleDiabetes2015
RAGE Suppresses ABCG1-Mediated Macrophage Cholesterol Efflux in Diabetes.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 67 citations in OpenAlex.
- Kidney-Vascular Metabolic Crosstalk: Altered Lipoproteins in CKD.Circulation research · 2026Review
- Article
- Glycated High-Density Lipoproteins Reduce Endothelial Phenotypic Expression of Monocyte-Derived Multipotential Cells in Early Type 2 Diabetes.Metabolites · 2026Article
- Role and mechanisms of vascular smooth muscle cell phenotypic transition in diabetic macrovascular complications.Biological research · 2026Review
- Molecular features and diagnostic modeling of synovium- and IPFP-derived OA macrophages in the inflammatory microenvironment via scRNA-seq and machine learning.Journal of orthopaedic surgery and research · 2025Article
- Resveratrol prevents gallstones in mice fed on a high fat diet via regulating PPAR-γ and SR-BI.Frontiers in pharmacology · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Advanced glycation end products promote meniscal calcification by activating the mTOR-ATF4 positive feedback loop.Experimental & molecular medicine · 2024Article
- DIAPH1-MFN2 interaction regulates mitochondria-SR/ER contact and modulates ischemic/hypoxic stress.Nature communications · 2023Article
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- Advanced Glycation End Products: A Sweet Flavor That Embitters Cardiovascular Disease.International journal of molecular sciences · 2022Review
- Glycation and a Spark of ALEs (Advanced Lipoxidation End Products) - Igniting RAGE/Diaphanous-1 and Cardiometabolic Disease.Frontiers in cardiovascular medicine · 2022Review
- Genomic Variants and Multilevel Regulation ofJournal of cardiovascular development and disease · 2021Review
- Persistent Effect of Advanced Glycated Albumin Driving Inflammation and Disturbances in Cholesterol Efflux in Macrophages.Nutrients · 2021Article
- Current Understanding of the Immunomodulatory Activities of High-Density Lipoproteins.Biomedicines · 2021Review
- High Density Lipoproteins and Diabetes.Cells · 2021Review
- HDL particle size is increased and HDL-cholesterol efflux is enhanced in type 1 diabetes: a cross-sectional study.Diabetologia · 2021Article
- Multi-Omics Comparison of the Spontaneous Diabetes Mellitus and Diet-Induced Prediabetic Macaque Models.Frontiers in pharmacology · 2021Article
- Potential Role of Protein Kinase C in the Pathophysiology of Diabetes-Associated Atherosclerosis.Frontiers in pharmacology · 2021Review
- Inflammation Meets Metabolism: Roles for the Receptor for Advanced Glycation End Products Axis in Cardiovascular Disease.Immunometabolism · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetes exacerbates cardiovascular disease, at least in part through suppression of macrophage cholesterol efflux and levels of the cholesterol transporters ATP binding cassette transporter A1 (ABCA1) and ABCG1. The receptor for advanced glycation end products (RAGE) is highly expressed in human and murine diabetic atherosclerotic plaques, particularly in macrophages. We tested the hypothesis that RAGE suppresses macrophage cholesterol efflux and probed the mechanisms by which RAGE downregulates ABCA1 and ABCG1. Macrophage cholesterol efflux to apolipoprotein A1 and HDL and reverse cholesterol transport to plasma, liver, and feces were reduced in diabetic macrophages through RAGE. In vitro, RAGE ligands suppressed ABCG1 and ABCA1 promoter luciferase activity and transcription of ABCG1 and ABCA1 through peroxisome proliferator-activated receptor-γ (PPARG)-responsive promoter elements but not through liver X receptor elements. Plasma levels of HDL were reduced in diabetic mice in a RAGE-dependent manner. Laser capture microdissected CD68(+) macrophages from atherosclerotic plaques of Ldlr(-/-) mice devoid of Ager (RAGE) displayed higher levels of Abca1, Abcg1, and Pparg mRNA transcripts versus Ager-expressing Ldlr(-/-) mice independently of glycemia or plasma levels of total cholesterol and triglycerides. Antagonism of RAGE may fill an important therapeutic gap in the treatment of diabetic macrovascular complications.
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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.