ReviewBiomedicines2023
Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 33 citations in OpenAlex.
- Immuno-Inflammatory Profiling and Complement Activation in Fabry Disease: A Cross-Sectional Study.International journal of molecular sciences · 2026Article
- Nrf2/NOX2 Pathway Dysregulation and Oxidative Stress Biomarkers in Gaucher Disease-Associated Parkinsonism: Insights Into a Potential Therapeutic Target.Journal of cellular and molecular medicine · 2026Article
- Metabolic differences in female adolescents with obsessive-compulsive disorder and trichotillomania: insights from plasma untargeted metabolomic analysis.BMC psychiatry · 2026Article
- Navigating the Ethereal Tightrope: The Nanogenerator Manipulates Neurons for Immune Equilibrium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Intrathecal delivery of AAVrh10-mHexa combined with anti-inflammatory treatment reduces neuropathological markers and extends the lifespan of mice with early-onset Tay-Sachs disease.Metabolic brain disease · 2026Article
- Interaction Between Microglial Lipid Droplet Metabolism and Immune Polarisation After Stroke: Mechanisms and Therapeutic Prospects.Cellular and molecular neurobiology · 2025Review
- Lysosomal acid lipase deficiency: The forgotten link between liver and cardiovascular disease.World journal of cardiology · 2025Review
- Central Roles of Glucosylceramide in Driving Cancer Pathogenesis.International journal of molecular sciences · 2025Review
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- Lysosomal LRRC8 complex impacts lysosomal pH, morphology, and systemic glucose metabolism.Science advances · 2025Article
- Fabry Disease Beyond Storage: The Role of Inflammation in Disease Progression.International journal of molecular sciences · 2025Review
- Molecular Diplomacy of Lipids in the War of Immunity: Bridging Rare and Common Disease Mechanisms.International journal of molecular sciences · 2025Article
- Combined treatment of Ketogenic diet and propagermanium reduces neuroinflammation in Tay-Sachs disease mouse model.Metabolic brain disease · 2025Article
- Enzyme Replacement Therapy in Mucopolysaccharidosis Type VII: A Three-Year Clinical Outcome Study of the First Taiwanese Case.Diagnostics (Basel, Switzerland) · 2025Article
- Extracellular Vesicles as Tools for Crossing the Blood-Brain Barrier to Treat Lysosomal Storage Diseases.Life (Basel, Switzerland) · 2025Review
- Unifying biology of neurodegeneration in lysosomal storage diseases.Journal of inherited metabolic disease · 2025Review
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- Gaucher disease type 3c: Expanding the clinical spectrum of an ultra-rare disease.JIMD reports · 2024Article
- Targeting GM2 Ganglioside Accumulation in Dementia: Current Therapeutic Approaches and Future Directions.Current molecular medicine · 2024Review
- Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysosomal storage diseases are a group of rare and ultra-rare genetic disorders caused by defects in specific genes that result in the accumulation of toxic substances in the lysosome. This excess accumulation of such cellular materials stimulates the activation of immune and neurological cells, leading to neuroinflammation and neurodegeneration in the central and peripheral nervous systems. Examples of lysosomal storage diseases include Gaucher, Fabry, Tay-Sachs, Sandhoff, and Wolman diseases. These diseases are characterized by the accumulation of various substrates, such as glucosylceramide, globotriaosylceramide, ganglioside GM2, sphingomyelin, ceramide, and triglycerides, in the affected cells. The resulting pro-inflammatory environment leads to the generation of pro-inflammatory cytokines, chemokines, growth factors, and several components of complement cascades, which contribute to the progressive neurodegeneration seen in these diseases. In this study, we provide an overview of the genetic defects associated with lysosomal storage diseases and their impact on the induction of neuro-immune inflammation. By understanding the underlying mechanisms behind these diseases, we aim to provide new insights into potential biomarkers and therapeutic targets for monitoring and managing the severity of these diseases. In conclusion, lysosomal storage diseases present a complex challenge for patients and clinicians, but this study offers a comprehensive overview of the impact of these diseases on the central and peripheral nervous systems and provides a foundation for further research into potential treatments.
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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 Socratic graph.