Modulation of OPC Mitochondrial Function by Inhibiting USP30 Promotes Their Differentiation.

ABSTRACT: Multiple lines of evidence indicate that mitochondrial dysfunction occurs in demyelinating diseases, such as multiple sclerosis (MS). Failure of remyelination is thought to be caused in part by a block of oligodendrocyte progenitor cell (OPC) differentiation into oligodendrocytes, which generate myelin sheaths around axons. The process of OPC differentiation requires a substantial amount of energy and high demand for ATP which is supplied through the mitochondria. In this study, we highlight mitochondrial gene expression changes during OPC differentiation in two murine models of remyelination and in human postmortem MS brains. Given these transcriptional alterations, we then investigate whether genetic alteration of USP30, a mitochondrial deubiquitinase, enhances OPC differentiation and my

SUBMITTER: Soung AL 

PROVIDER: S-EPMC11845845 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature