ReviewAtherosclerosis2024
RAGE/DIAPH1 and atherosclerosis through an evolving lens: Viewing the cell from the "Inside - Out".
Review in Atherosclerosis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
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
8 citing papers in PubMed.
- Advanced glycation end products and RAGE signaling in diabetic cardiomyopathy: distinct mechanisms, human evidence, and translational barriers.Frontiers in cardiovascular medicine · 2026Review
- 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
- Facile Synthesis ofInternational journal of molecular sciences · 2025Article
- Polymeric Nanomaterials for Atherosclerosis Diagnosis and Treatment.Polymer science & technology (Washington, D.C.) · 2025Review
- A multi-trait genome-wide association study of coronary artery disease and subclinical atherosclerosis traits.Research square · 2025Article
- Pathological role of RAGE underlying progression of various diseases: its potential as biomarker and therapeutic target.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Background and aims: In hyperglycemia, inflammation, oxidative stress and aging, Damage Associated Molecular Patterns (DAMPs) accumulate in conditions such as atherosclerosis. Binding of DAMPs to receptors such as the receptor for advanced glycation end products (RAGE) activates signal transduction cascades that contribute to cellular stress. The cytoplasmic domain (tail) of RAGE (ctRAGE) binds to the formin Diaphanous1 (DIAPH1), which is important for RAGE signaling. This Review will detail the evidence linking the RAGE/DIAPH1 signaling pathway to atherosclerosis and envisages future therapeutic opportunities from the "inside-out" point of view in affected cells. Methods: PubMed was searched using a variety of search terms, including "receptor for advanced glycation end products" along with various combinations including "and atherosclerosis," "soluble RAGE and atherosclerosis," "statins and RAGE," "PPAR and RAGE" and "SGLT2 inhibitor and RAGE." Results: In non-diabetic and diabetic mice, antagonism or global deletion of Conclusions: Efforts to target RAGE/DIAPH1 signaling through a small molecule antagonist therapeutic strategy hold promise to quell accelerated atherosclerosis in diabetes and in other forms of cardiovascular disease.
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What OpenQuestion holds
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.