Neural cell death is the main feature of all retinal degenerative disorders that lead to blindness. Despite therapeutic advances, progression of retinal disease cannot always be prevented, and once neuronal cell damage occurs, visual loss cannot be reversed. Recent research in the stem cell field, and the identification of Müller glia with stem cell characteristics in the human eye, have provided hope for the use of these cells in retinal therapies to restore vision. Müller glial cells, which are the major structural cells of the retina, play a very important role in retinal homeostasis during health and disease. They are responsible for the spontaneous retinal regeneration observed in zebrafish and lower vertebrates during early postnatal life, and despite the presence of Müller glia with stem cell characteristics in the adult mammalian retina, there is no evidence that they promote regeneration in humans. Like many other stem cells and neurons derived from pluripotent stem cells, Müller glia with stem cell potential do not differentiate into retinal neurons or integrate into the retina when transplanted into the vitreous of experimental animals with retinal degeneration. However, despite their lack of integration, grafted Müller glia have been shown to induce partial restoration of visual function in spontaneous or induced experimental models of photoreceptor or retinal ganglion cell damage. This improvement in visual function observed after Müller cell transplantation has been ascribed to the release of neuroprotective factors that promote the repair and survival of damaged neurons. Due to the development and availability of pluripotent stem cell lines for therapeutic uses, derivation of Müller cells from retinal organoids formed by iPSC and ESC has provided more realistic prospects for the application of these cells to retinal therapies. Several opportunities for research in the regenerative field have also been unlocked in recent years due to a better understanding of the genomic and proteomic profiles of the developing and regenerating retina in zebrafish, providing the basis for further studies of the human retina. In addition, the increased interest on the nature and function of cellular organelle release and the characterization of molecular components of exosomes released by Müller glia, may help us to design new approaches that could be applied to the development of more effective treatments for retinal degenerative diseases.

神经细胞死亡是所有导致失明的视网膜退行性疾病的主要特征。尽管治疗取得了进步，但视网膜疾病的进展并不总是可以预防，一旦发生神经元细胞损伤，视力丧失就无法逆转。最近在干细胞领域的研究，以及在人眼中鉴定出具有干细胞特征的 Müller 胶质细胞，为将这些细胞用于视网膜治疗以恢复视力提供了希望。Müller 胶质细胞是视网膜的主要结构细胞，在健康和疾病期间的视网膜稳态中发挥着非常重要的作用。它们负责在斑马鱼和低等脊椎动物出生后早期观察到的自发视网膜再生，尽管在成年哺乳动物视网膜中存在具有干细胞特征的 Müller 胶质细胞，没有证据表明它们可以促进人类再生。与许多其他源自多能干细胞的干细胞和神经元一样，具有干细胞潜能的 Müller 胶质细胞在移植到视网膜变性实验动物的玻璃体中时不会分化成视网膜神经元或整合到视网膜中。然而，尽管它们缺乏整合，但移植的 Müller 神经胶质已被证明可以在感光细胞或视网膜神经节细胞损伤的自发或诱导实验模型中诱导视觉功能的部分恢复。Müller 细胞移植后观察到的视觉功能改善归因于神经保护因子的释放，这些因子促进了受损神经元的修复和存活。由于用于治疗用途的多能干细胞系的开发和可用性，从由 iPSC 和 ESC 形成的视网膜类器官中衍生出 Müller 细胞，为将这些细胞应用于视网膜治疗提供了更现实的前景。近年来，由于对斑马鱼发育和再生视网膜的基因组和蛋白质组学特征有了更好的了解，再生领域的一些研究机会也被释放，为进一步研究人类视网膜提供了基础。此外，对细胞器释放的性质和功能以及 Müller 神经胶质细胞释放的外泌体分子成分表征的兴趣增加，可能有助于我们设计新方法，用于开发更有效的视网膜退行性疾病治疗方法.