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Abstract
Myelin, produced by oligodendrocytes (OLs), is essential for rapid neural signaling, but is often lost in CNS injuries and diseases like multiple sclerosis (MS). Remyelination requires oligodendrocyte progenitor cells (OPCs) to mature, yet this process frequently fails due to inhibitory molecules in lesions. This study identifies hyaluronidase-generated hyaluronan (HA) fragments as key inhibitors of OL maturation. PH20, a hyaluronidase found in chronic MS lesions and EAE models, emerges as a potential therapeutic target. Findings suggest controlled HA catabolism influences OPC proliferation, migration, and neural repair, highlighting extracellular matrix regulation as critical for white matter regeneration.