ReviewNature reviews. Neurology2023
Inflammation in multiple sclerosis: consequences for remyelination and disease progression.
Review in Nature reviews. Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
64 citing papers in PubMed, 103 citations in OpenAlex.
- Selective inhibition of TLR2 stimulates the maturation of oligodendroglial progenitor cells to oligodendrocytes.NeuroImmune pharmacology and therapeutics · 2026Article
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Kappa Free Light Chain for Diagnosis and Neurofilament Light Chain for Prognosis in Autoimmune Encephalitis.Neurology(R) neuroimmunology & neuroinflammation · 2026Observational
- Targeting progressive multiple sclerosis: Toward mechanism-informed precision medicine.Journal of internal medicine · 2026Review
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- Cerebral dopamine neurotrophic factor for spinal cord injury: Targeting JNK1 to relieve neuroinflammation and improve neural repair.Neural regeneration research · 2026Article
- Emerging Role of BTK Inhibitors in Multiple Sclerosis: From Immunobiology to Clinical Translation.Brain sciences · 2026Review
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- [XVII Post-ECTRIMS Meeting: Review of the New Developments Presented at the 2024 ECTRIMS Congress (I)].Revista de neurologia · 2026Review
- The GPR17 agonist galinex restores oligodendrocyte maturation under inflammatory conditions.Frontiers in pharmacology · 2026Article
- The oxidative stress-inflammation self-perpetuating cycle in multiple sclerosis: from mechanisms to emerging antioxidant strategies.Frontiers in pharmacology · 2026Review
- Motor tract lesion mapping from the brain to the lower spinal cord in people with relapsing-remitting multiple sclerosis: exploring the association between lesion severity and functional consequences by limb.Brain communications · 2026Article
- Unraveling multiple sclerosis: a hidden interaction between intestinal microbiota and host lipid metabolism.Gut microbes · 2025Review
- MLKL Modulates Necroptosis and Neuroinflammation in a Mouse Model of MS.Inflammation · 2025Article
- Age-impaired remyelination is associated with dysregulated microglial transitions.Nature communications · 2025Article
- Local control of T cell fate in lymph nodes safely and durably reverses myelin-driven autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Selective inhibition of mitochondrial Kv1.3 prevents and alleviates multiple sclerosis in vivo.EMBO molecular medicine · 2025Article
- Development of a Human Preclinical Platform for the Identification of Neuroprotective Compounds.The European journal of neuroscience · 2025Article
4 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the large number of immunomodulatory or immunosuppressive treatments available to treat relapsing-remitting multiple sclerosis (MS), treatment of the progressive phase of the disease has not yet been achieved. This lack of successful treatment approaches is caused by our poor understanding of the mechanisms driving disease progression. Emerging concepts suggest that a combination of persisting focal and diffuse inflammation within the CNS and a gradual failure of compensatory mechanisms, including remyelination, result in disease progression. Therefore, promotion of remyelination presents a promising intervention approach. However, despite our increasing knowledge regarding the cellular and molecular mechanisms regulating remyelination in animal models, therapeutic increases in remyelination remain an unmet need in MS, which suggests that mechanisms of remyelination and remyelination failure differ fundamentally between humans and demyelinating animal models. New and emerging technologies now allow us to investigate the cellular and molecular mechanisms underlying remyelination failure in human tissue samples in an unprecedented way. The aim of this Review is to summarize our current knowledge regarding mechanisms of remyelination and remyelination failure in MS and in animal models of the disease, identify open questions, challenge existing concepts, and discuss strategies to overcome the translational roadblock in the field of remyelination-promoting therapies.
Indexed as
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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.