ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2018
sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by inhibiting RAGE-NFκB-NLRP3 activation.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
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- NLRP3 inflammasome in cardiovascular diseases: molecular mechanisms and advances in targeted drug research.Frontiers in immunology · 2026Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 2025Review
- Long noncoding RNA AK144717 exacerbates pathological cardiac hypertrophy through modulating the cellular distribution of HMGB1 and subsequent DNA damage response.Cellular and molecular life sciences : CMLS · 2024Article
- Role of the receptor for advanced glycation end products in the severity of SARS-CoV-2 infection in diabetic patients.Diabetology international · 2024Review
- Enhanced Cardiomyocyte NLRP3 Inflammasome-Mediated Pyroptosis Promotes d-Galactose-Induced Cardiac Aging.Journal of the American Heart Association · 2024Article
- Cardiac hypertrophy that affects hyperthyroidism occurs independently of the NLRP3 inflammasome.Pflugers Archiv : European journal of physiology · 2024Article
- Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions.MedComm · 2024Review
- The role of pyroptosis in heart failure and related traditional chinese medicine treatments.Frontiers in pharmacology · 2024Review
- Activation of the High Mobility Group Box 1/Receptor for Advanced Glycation Endproducts /NOD-like Receptor Family Pyrin Domain-Containing 3 Axis Under Chronic Intermittent Hypoxia Induction Promotes the Progression of Atherosclerosis in ApoEJournal of the American Heart Association · 2023Article
- A Low Concentration of Citreoviridin Prevents Both Intracellular Calcium Deposition in Vascular Smooth Muscle Cell and Osteoclast Activation In Vitro.Molecules (Basel, Switzerland) · 2023Article
- Recombinant human angiotensin-converting enzyme 2 plays a protective role in mice with sepsis-induced cardiac dysfunction through multiple signaling pathways dependent on converting angiotensin II to angiotensin 1-7.Annals of translational medicine · 2023Article
- Soluble receptors for advanced glycation end-products prevent unilateral ureteral obstruction-induced renal fibrosis.Frontiers in pharmacology · 2023Article
- Cardiac Remodeling in Heart Failure: Role of Pyroptosis and Its Therapeutic Implications.Frontiers in cardiovascular medicine · 2022Review
- BRD4 Silencing Protects Angiotensin II-Induced Cardiac Hypertrophy by Inhibiting TLR4/NF-Cardiology research and practice · 2022Article
- Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.Life sciences · 2021Review
- Chronic stress promotes acute myeloid leukemia progression through HMGB1/NLRP3/IL-1β signaling pathway.Journal of molecular medicine (Berlin, Germany) · 2021Article
- SARS-CoV-2 Entry Receptor ACE2 Is Expressed on Very Small CD45Stem cell reviews and reports · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
OBJECTIVE AND
designThe receptor for advanced glycation endproducts (RAGE) is an innate immunity receptor that has been implicated in the pathogenesis of atherosclerotic cardiovascular disease. However, the possibility that RAGE-mediated signaling is involved in angiotensin II (Ang II)-induced cardiac left ventricular hypertrophy has yet to be investigated. We therefore determined whether RAGE has a role in regulating pathological cardiac hypertrophy. MATERIALS AND SUBJECTS: Protein abundance was estimated using Western blotting and intracellular ROS level and phospho-p65 were detected using fluorescence microscopy. Enzyme-linked immunosorbent assay was used to detect HMGB1 and IL-1β. All in vitro experiments were performed using H9C2 cells. TREATMENTS: To induce cardiomyocyte hypertrophy, 300 nM Ang II was treated for 48 h and 2 µg/ml sRAGE was treated 1 h prior to addition of Ang II.
resultssRAGE attenuated Ang II-induced cardiomyocyte hypertrophy by downregulating RAGE and angiotensin II type 1 receptor expression. Secretion levels of high motility group box 1 and interleukin-1β, estimated from a cell culture medium, were significantly reduced by sRAGE. Activated PKCs and ERK1/2, important signals in left ventricular hypertrophy (LVH) development, were downregulated by sRAGE treatment. Furthermore, we found that nuclear factor-κB and NOD-like receptor protein 3 (NLRP3) were associated with RAGE-mediated cardiomyocyte hypertrophy.
conclusionsIn the context of these results, we conclude that RAGE induces cardiac hypertrophy through the activation of the PKCs-ERK1/2 and NF-κB-NLRP3-IL1β signaling pathway, and suggest that RAGE-NLRP3 may be an important mediator of Ang II-induced cardiomyocyte hypertrophy. In addition, we determined that inhibition of RAGE activation with soluble RAGE (sRAGE) has a protective effect on Ang II-induced cardiomyocyte hypertrophy.
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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.