MicroRNAs in oligodendrocyte development and remyelination

Oligodendrocytes are the glial cells responsible for the formation of myelin around axons of the central nervous system (CNS). Myelin is an insulating layer that allows electrical impulses to transmit quickly and efficiently along neurons. If myelin is damaged, as in chronic demyelinating disorders such as multiple sclerosis (MS), these impulses slow down. Remyelination by oligodendrocytes is often ineffective in MS, in part because of the failure of oligodendrocyte precursor cells (OPCs) to differentiate into mature, myelinating oligodendrocytes. The process of oligodendrocyte differentiation is tightly controlled by several regulatory networks involving transcription factors, intracellular signaling pathways, and extrinsic cues. Understanding the factors that regulate oligodendrocyte development is essential for the discovery of new therapeutic strategies capable of enhancing remyelination. Over the past decade, microRNAs (miRNAs) have emerged as key regulators of oligodendrocyte development, exerting effects on cell specification, proliferation, differentiation, and myelination. This article will review the role of miRNAs on oligodendrocyte biology and discuss their potential as promising therapeutic tools for remyelination.

Automated summary

Oligodendrocytes play a crucial role in the formation of myelin in the central nervous system. Demyelinating disorders like multiple sclerosis (MS) result in damaged myelin and slower transmission of electrical impulses. The failure of oligodendrocyte precursor cells (OPCs) to differentiate into mature, myelinating oligodendrocytes hinders remyelination in MS. Understanding the regulation of oligodendrocyte development is important for developing new therapeutic strategies. MicroRNAs (miRNAs) have emerged as key regulators of oligodendrocyte biology, influencing cell specification, proliferation, differentiation, and myelination. This article explores the role of miRNAs in oligodendrocyte biology and their potential as therapeutic tools for remyelination.