Oligodendrocytes are essential for the development, function, and health of the vertebrate central nervous system. These cells maintain axon myelination to ensure saltatory propagation of action potentials. Oligodendrocyte develops from neural progenitor cells, in a step-wise process that involves oligodendrocyte precursor specification, proliferation, and differentiation. The lineage progression requires coordination of transcriptional and epigenetic circuits to mediate the stage-specific intricacies of oligodendrocyte development. Epigenetic mechanisms involve DNA methylation, histone modifications, ATP-dependent chromatin remodeling, and non-coding RNA modulation that regulate the chromatin state over regulatory genes, which must be expressed or repressed to establish oligodendrocyte identity and lineage progression. In this review, we will focus on epigenetic programming associated with histone modification enzymes, chromatin remodeling, and non-coding RNAs that regulate oligodendrocyte lineage progression, and discuss how these mechanisms might be harnessed to induce myelin repair for treatment of demyelinating diseases such as multiple sclerosis.

少突胶质细胞对于脊椎动物中枢神经系统的发育，功能和健康至关重要。这些细胞维持轴突的髓鞘形成，以确保动作电位的盐分传播。少突胶质细胞是由神经祖细胞发育而成的，是一个逐步过程，涉及少突胶质细胞前体的特性，增殖和分化。沿袭进程需要转录和表观遗传电路的协调，以介导少突胶质细胞发育的阶段特定的复杂性。表观遗传机制涉及DNA甲基化，组蛋白修饰，ATP依赖的染色质重塑和非编码RNA调节，这些调节调节染色质状态超过调节基因，必须将其表达或抑制以建立少突胶质细胞身份和谱系进展。在这篇评论中，