ArticleChembiochem : a European journal of chemical biology2023
Modulating the RAGE-Induced Inflammatory Response: Peptoids as RAGE Antagonists.
Article in Chembiochem : a European journal of chemical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The RAGE-Ferroptosis Axis Drives Oxidative Stress-Associated Inflammatory Lung Injury in Viral Infection.Antioxidants (Basel, Switzerland) · 2026Article
- Advanced glycation end products and RAGE signaling in diabetic cardiomyopathy: distinct mechanisms, human evidence, and translational barriers.Frontiers in cardiovascular medicine · 2026Review
- S100B in brain-gut-liver crosstalk: from glial activation to multiorgan inflammation.Frontiers in immunology · 2026Review
- Identifying RAGE inhibitors as potential therapeutics for Alzheimer's disease via integrated in-silico approaches.Scientific reports · 2025Article
- Article
- Rationally Designed Peptoid Inhibitors of Amyloid-β Oligomerization.Chembiochem : a European journal of chemical biology · 2024Article
- Anti-Neuroinflammatory Effects of a Macrocyclic Peptide-Peptoid Hybrid in Lipopolysaccharide-Stimulated BV2 Microglial Cells.International journal of molecular sciences · 2024Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
While the primary pathology of Alzheimer's disease (AD) is defined by brain deposition of amyloid-β (Aβ) plaques and tau neurofibrillary tangles, chronic inflammation has emerged as an important factor in AD etiology. Upregulated cell surface expression of the receptor for advanced glycation end-products (RAGE), a key receptor of innate immune response, is reported in AD. In parallel, RAGE ligands, including Aβ aggregates, HMGB1, and S100B, are elevated in AD brain. Activation of RAGE by these ligands triggers release of inflammatory cytokines and upregulates cell surface RAGE. Despite such observation, there are currently no therapeutics that target RAGE for treatment of AD-associated neuroinflammation. Peptoids, a novel class of potential AD therapeutics, display low toxicity, facile blood-brain barrier permeability, and resistance to proteolytic degradation. In the current study, peptoids were designed to mimic Aβ, a ligand that binds the V-domain of RAGE, and curtail RAGE inflammatory activation. We reveal the nanomolar binding capability of peptoids JPT1 and JPT1a to RAGE and demonstrate their ability to attenuate lipopolysaccharide-induced pro-inflammatory cytokine production as well as upregulation of RAGE cell surface expression. These results support RAGE antagonist peptoid-based mimics as a prospective therapeutic strategy to counter neuroinflammation in AD and other neurodegenerative diseases.
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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.