ReviewMolecules (Basel, Switzerland)2022
Therapeutic Potential of Targeting the HMGB1/RAGE Axis in Inflammatory Diseases.
Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Role of Cellular-Ferroptosis-Mediated HMGB1 Nuclear Translocation in Indium-Tin-Oxide-Nanoparticle-Induced Inflammatory Lung Injury.Environment & health (Washington, D.C.) · 2026Article
- Advances in electroacupuncture for perioperative neurocognitive disorders: mechanisms and clinical evidence.Chinese medicine · 2026Review
- Cardiorenal Protective Effects of Finerenone in Patients with Type 2 Diabetes Mellitus.Archives of internal medicine research · 2026Article
- Article
- Effects of Lactate on Improving Cognitive Function and Survival Rate in a Mouse Model of Post-Sepsis Cognitive Impairment.Actas espanolas de psiquiatria · 2026Article
- Serum HMGB1 as a biomarker and predictive model for pediatric septic shock: a cohort study.Translational pediatrics · 2026Article
- Randomized controlled trial of intraosseous access vs. intravenous access in traumatic hemorrhagic shock: Effects on inflammation, hematopoiesis, and coagulation.Journal of medical biochemistry · 2026Article
- R-α-Lipoic Acid Attenuates Acetaminophen-Induced Acute Liver Injury by Reducing Oxidative Stress, Inflammation, and Mitochondrial Damage in Mice.Drug design, development and therapy · 2026Article
- EnterotoxigenicFrontiers in immunology · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Article
- HMGB1 as a Key Modulator in Nasal Inflammatory Disorders: A Narrative Review.Journal of clinical medicine · 2025Review
- Targeting RAGE-signaling pathways in the repair of rotator-cuff injury.Molecular and cellular biochemistry · 2025Review
- The Impact of Recreational Diving to a Depth of 40 m on Selected Intracellular DAMPs.International journal of molecular sciences · 2025Article
- Article
- MiR-216a-5p protects against high glucose-induced HMC injury by targeting the HMGB1/RAGE signaling pathway.Frontiers in endocrinology · 2025Article
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Early serum biomarkers to characterise different phenotypes of primary graft dysfunction after lung transplantation: a systematic scoping review.ERJ open research · 2024Article
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
- Computational Biology in the Discovery of Biomarkers in the Diagnosis, Treatment and Management of Cardiovascular Diseases.Cardiology and cardiovascular medicine · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
High mobility group box 1 (HMGB1) is a nuclear protein that can interact with a receptor for advanced glycation end-products (RAGE; a multi-ligand immunoglobulin receptor) and mediates the inflammatory pathways that lead to various pathological conditions, such as cancer, diabetes, neurodegenerative disorders, and cardiovascular diseases. Blocking the HMGB1/RAGE axis could be an effective therapeutic approach to treat these inflammatory conditions, which has been successfully employed by various research groups recently. In this article, we critically review the structural insights and functional mechanism of HMGB1 and RAGE to mediate inflammatory processes. More importantly, current perspectives of recent therapeutic approaches utilized to inhibit the communication between HMGB1 and RAGE using small molecules are also summarized along with their clinical progression to treat various inflammatory disorders. Encouraging results are reported by investigators focusing on HMGB1/RAGE signaling leading to the identification of compounds that could be useful in further clinical studies. We highlight the current gaps in our knowledge and future directions for the therapeutic potential of targeting key molecules in HMGB1/RAGE signaling in the pathophysiology of inflammatory 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.