ArticleThe Journal of clinical investigation2019
Transactivation of RAGE mediates angiotensin-induced inflammation and atherogenesis.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 82 citations in OpenAlex.
- RAGE phosphorylation by CK2 in human epithelial cell model: Modulation of connexin 43 expression.iScience · 2026Article
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- Microplastic exposure elicits sex-specific atherosclerosis development in lean low-density lipoprotein receptor-deficient mice.Environment international · 2025Article
- Article
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Type 1 diabetes mellitus prevention: present and future.Nature reviews. Endocrinology · 2025Review
- miR-129-5p regulates HMGB1/RAGE axis to inhibit pyroptosis and ameliorate cervical epithelial cell deterioration.European journal of histochemistry : EJH · 2025Article
- Semaglutide: a key medication for managing cardiovascular-kidney-metabolic syndrome.Future cardiology · 2025Review
- Review
- RAGE deficiency ameliorates abdominal aortic aneurysm progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- Role of the receptor for advanced glycation end products in the severity of SARS-CoV-2 infection in diabetic patients.Diabetology international · 2024Review
- Paternal hypercholesterolemia elicits sex-specific exacerbation of atherosclerosis in offspring.JCI insight · 2024Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Unraveling the SARS-CoV-2 spike protein long-term effect on neuro-PASC.Frontiers in cellular neuroscience · 2024Article
- When It Comes to COVID-19, Inflammation Is All the RAGE.American journal of respiratory cell and molecular biology · 2023Article
- RAGE Is a Receptor for SARS-CoV-2 N Protein and Mediates N Protein-induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2023Article
- Recent Advances in Anti-Atherosclerosis and Potential Therapeutic Targets for Nanomaterial-Derived Drug Formulations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- RAGE ablation attenuates glioma progression and enhances tumor immune responses by suppressing galectin-3 expression.Neuro-oncology · 2023Article
- PANDORA-Seq unveils the hidden small noncoding RNA landscape in atherosclerosis of LDL receptor-deficient mice.Journal of lipid research · 2023Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the type 1 angiotensin II receptor (AT1) triggers proinflammatory signaling through pathways independent of classical Gq signaling that regulate vascular homeostasis. Here, we report that the AT1 receptor preformed a heteromeric complex with the receptor for advanced glycation endproducts (RAGE). Activation of the AT1 receptor by angiotensin II (Ang II) triggered transactivation of the cytosolic tail of RAGE and NF-κB-driven proinflammatory gene expression independently of the liberation of RAGE ligands or the ligand-binding ectodomain of RAGE. The importance of this transactivation pathway was demonstrated by our finding that adverse proinflammatory signaling events induced by AT1 receptor activation were attenuated when RAGE was deleted or transactivation of its cytosolic tail was inhibited. At the same time, classical homeostatic Gq signaling pathways were unaffected by RAGE deletion or inhibition. These data position RAGE transactivation by the AT1 receptor as a target for vasculoprotective interventions. As proof of concept, we showed that treatment with the mutant RAGE peptide S391A-RAGE362-404 was able to inhibit transactivation of RAGE and attenuate Ang II-dependent inflammation and atherogenesis. Furthermore, treatment with WT RAGE362-404 restored Ang II-dependent atherogenesis in Ager/Apoe-KO mice, without restoring ligand-mediated signaling via RAGE, suggesting that the major effector of RAGE activation was its transactivation.
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