Remyelination is a physiological response to demyelinating events aiming to restore saltatory conduction and preserve axonal integrity. Resident oligodendrocyte precursor cells (OPC) of the CNS tissue under appropriate conditions are mobilized to proliferate, migrate, and differentiate, in order to produce new myelin sheaths in the demyelinated lesion. In multiple sclerosis (MS), the most common immune-mediated demyelinating disease, remyelination efficiency declines with increasing age and disease duration. As myelin regeneration attempts in clinical trials so far are scarce, and have been met with limited success, the need to explore new remyelinating strategies is more compelling. Recently, ageing and cellular senescence have been implicated to the pathophysiology of a number of neurodegenerative diseases, including multiple sclerosis. Evidence on OPC senescence brings forward the possibility of exploiting cellular senescence as a possible target for promoting the endogenous remyelinating capacity of the CNS. Here we discuss the data indicating how cellular senescence affects remyelination, and the putative benefits to be drawn through the use of senolytic or senomorphic therapies targeting senescent cell populations in MS.

髓鞘再生是对脱髓鞘事件的生理反应，旨在恢复跳跃传导并保持轴突完整性。在适当条件下，CNS 组织的常驻少突胶质细胞前体细胞 (OPC) 被动员增殖、迁移和分化，以便在脱髓鞘病变中产生新的髓鞘。在多发性硬化症 (MS) 中，最常见的免疫介导的脱髓鞘疾病，髓鞘再生效率随着年龄和疾病持续时间的增加而下降。由于迄今为止临床试验中髓鞘再生的尝试很少，并且成功率有限，因此探索新的髓鞘再生策略的需求更加迫切。最近，衰老和细胞衰老与许多神经退行性疾病的病理生理学有关，包括多发性硬化症。OPC 衰老的证据提出了利用细胞衰老作为促进中枢神经系统内源性髓鞘再生能力的可能目标的可能性。在这里，我们讨论了表明细胞衰老如何影响髓鞘再生的数据，以及通过使用针对 MS 中衰老细胞群的衰老溶解或衰老疗法获得的假定益处。