ReviewJournal of neurochemistry2025
Platelets During Myelin Repair in Multiple Sclerosis: Friend or Foe?
Review in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The Neurovascular Niche: A Gathering Venue for Neuroinflammation and Remyelination in Multiple Sclerosis.Acta physiologica (Oxford, England) · 2026Review
- Platelets During Myelin Repair in Multiple Sclerosis: Friend or Foe?Journal of neurochemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune neuroinflammatory demyelinating disease of the central nervous system (CNS) that affects more than 2.5 million people worldwide. Remyelination represents a robust regenerative response to myelin damage; however, during the later stages of MS, this process largely fails. Upon demyelination, oligodendrocyte progenitor cells (OPCs) proliferate, migrate, and differentiate into mature remyelinating oligodendrocytes. Why does remyelination fail in MS? Platelets are small, oval, anucleate cells that circulate in the bloodstream and form a hemostatic plug to stop blood leakage upon endothelial damage. Platelet function is not restricted to hemostasis; they also display tissue-regenerative activities. Here, we review evidence suggesting that platelets act as modulators of OPC function during remyelination. Additionally, we describe platelet alterations associated with MS that may contribute to remyelination failure. Finally, we highlighted our previous study that addressed these issues. This study showed that in response to myelin damage, platelets transiently accumulate within the lesion. Interestingly, platelet depletion leads to a reduction in OPC differentiation, hindering remyelination. In vitro studies revealed that transient exposure to platelets boosts OPC differentiation, whereas sustained exposure to platelets suppresses this beneficial effect. Consistent with this observation, in an in vivo model of thrombocytosis (Calr
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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.