ArticleJournal of neuroinflammation2019
Therapeutic blockade of HMGB1 reduces early motor deficits, but not survival in the SOD1
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.
- The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review.Current neuropharmacology · 2022Pooled it
- Antibody-Based Therapeutic Interventions for Amyotrophic Lateral Sclerosis: A Systematic Literature Review.Frontiers in neuroscience · 2021Pooled it
- Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026Review
- HMGB1 functional plasticity in neurodegenerative diseases and its translational implications.Frontiers in immunology · 2026Review
- Desloratadine alleviates ALS-like pathology in hSOD1Acta pharmacologica Sinica · 2024Article
- Novel insights into RAGE signaling pathways during the progression of amyotrophic lateral sclerosis in RAGE-deficient SOD1 G93A mice.PloS one · 2024Article
- Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases.Current drug targets · 2024Review
- Connexin 30 Deficiency Ameliorates Disease Progression at the Early Phase in a Mouse Model of Amyotrophic Lateral Sclerosis by Suppressing Glial Inflammation.International journal of molecular sciences · 2022Article
- Molecular mechanisms of developmental pathways in neurological disorders: a pharmacological and therapeutic review.Open biology · 2022Review
- The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice.International journal of molecular sciences · 2022Article
- HMGB1 in nervous system diseases: A common biomarker and potential therapeutic target.Frontiers in neurology · 2022Review
- The role of immune-mediated alterations and disorders in ALS disease.Human immunology · 2021Review
- Single-cell deconstruction of post-sepsis skeletal muscle and adipose tissue microenvironments.Journal of cachexia, sarcopenia and muscle · 2020Article
- Absence of Receptor for Advanced Glycation End Product (RAGE) Reduces Inflammation and Extends Survival in the hSOD1Molecular neurobiology · 2020Article
- Targeting Inflammation Driven by HMGB1.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing neurodegenerative disease without effective treatment. The receptor for advanced glycation end products (RAGE) and the toll-like receptor (TLR) system are major components of the innate immune system, which have been implicated in ALS pathology. Extracellularly released high-mobility group box 1 (HMGB1) is a pleiotropic danger-associated molecular pattern (DAMP), and is an endogenous ligand for both RAGE and TLR4.
methodsThe present study examined the effect of HMGB1 inhibition on disease progression in the preclinical SOD1
resultsWe found that chronic intraperitoneal dosing of the anti-HMGB1 antibody to SOD1
conclusionsIn summary, our results indicate that therapeutic targeting of an extracellular DAMP, HMGB1, improves early motor dysfunction, but overall has limited efficacy in the SOD1
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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.