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Müller细胞是视网膜主要的神经胶质细胞，对于维持视网膜稳态有重要作用。视网膜损伤后，斑马鱼Müller细胞可以通过重编程进入细胞周期增生并分化为神经元，促进视网膜完成再生修复。高等动物Müller细胞的这一能力几乎消失，导致视网膜损伤后神经元无法再生，最终造成视功能减退，甚至丢失。研究发现，虽然视网膜损伤后Müller细胞重编程过程在高等动物中不能自发激活，但可以通过诱导增强其重编程能力并实现其向神经元的转分化。这种神经元再生潜能使Müller细胞在高等动物视网膜修复再生中极有应用前景。本文围绕Müller细胞转分化为神经元的最新研究进展，从Müller细胞起源及生理病理状态、重编程机制、哺乳动物Müller细胞向神经元转分化的诱导方式、限制Müller细胞转分化为神经元的因素4个方面展开，并对Müller细胞重编程参与视网膜再生的优势与前景以及目前存在的问题进行总结。“,”Müller glia, the major type of glial cells in retina, is crucial for maintaining retinal homeostasis.Although Müller cells have the features to re-enter into the cell cycle and differentiate into neural cells for promoting retinal regeneration after retinal damage in zebrafish, these features are rigorously restricted in higher animals.It has been reported that the reprogramming of Müller cells cannot be activated spontaneously in higher animals, but the reprogramming ability and transdifferentiation to neuron can be achieved by induction.The neurogenic potential of mammalian Müller glia makes it promising in restoring retinal regeneration.In this article, we review the progresses of Müller glia-to-neuron transdifferentiation with respect of the origin, and summarize the pathophysiology characters of Müller glia, mechanisms of reprogramming, methods of inducing mammalian Müller glia to neuron and factors limiting Müller glia-to-neuron in higher animals.Besides, we propose the advantages as well as the current challenges of Müller glia-to-neuron transdifferentiation.