ArticleJournal of neuroinflammation2025
Dihydroartemisinin enhances remyelination by switching microglia to the reparative phenotype.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- Zuo Gui Wan Promotes Remyelination in Multiple Sclerosis by Attenuating MAPK-Mediated Microglial M1 Polarization, an Integrated Network Pharmacology and Experimental Validation Study.Journal of inflammation research · 2026Article
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
backgroundBoosting myelin repair is widely recognized as one of the most powerful approaches for demyelinating therapy, essentially contributing to the recovery of neurological functions. Maintaining immune homeostasis in microglia is a prerequisite for creating a reparative environment for myelin. Dihydroartemisinin (DHA) is clinically effective in reshaping immunological status and implies potential in treating demyelinating disease. However, its relevance to pro-remyelination remains unclear.
methodsWe first evaluated the effects of DHA on neurofunctional recovery and white matter integrity in chronic experimental autoimmune encephalomyelitis (EAE), an ideal model for secondary progressive multiple sclerosis (SPMS) characterized by remyelination deficiency. Single-cell sequencing and microglial depletion with PLX3397 in vivo were used to reveal the dependency between DHA and microglia. The effect of DHA on the reparative phenotype of microglia, particularly on cholesterol recycling and differentiation of oligodendrocyte progenitor cells (OPCs), was evaluated in microglia-OPCs unit either in vitro or in vivo challenged with myelin debris. Finally, to broaden the clinical application for DHA in myelin repair, it was tested in the cuprizone (CPZ) model which shows remyelination failure, a condition common in various neurodegenerative diseases.
resultsWe demonstrated for the first time that DHA enhanced white matter integrity and OPCs proliferation and differentiation. This effect is dependent on the transition of microglia to a reparative phenotype. Specifically, DHA increased the secretion of inflammatory-resolving and neurotrophic cytokines. It further functionalized cholesterol recycling and provided metabolic support for myelin regeneration predominantly mediated by liver X receptor (LXR) in microglia. This was evidenced by the promotion of myelin debris uptake, cholesterol catabolism, efflux and transport. Notably, DHA promoted remyelination and neurological functional recovery in CPZ-induced demyelinating model, supporting its potential application in neurodegenerative diseases featuring insufficient remyelination.
conclusionBy highlighting the importance of microglia in promoting myelin regeneration, our study proved DHA as a promising candidate for promoting remyelination.
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