The regulatory role of mitochondrial quality control and post-translational modification in ganglion cell injury caused by retinal ischemia–reperfusion

Abstract Retinal ganglion cell injury is an irreversible common pathological process caused by retinal ischemia–reperfusion resulting from various ocular diseases, which can lead to vision loss and blindness. The normal functioning of retinal ganglion cells depends on the synergistic effect of mitochondria and other organelles; these organelles regulate multiple pathophysiological processes, including mitophagy, mitochondrial dynamics, oxidative stress, neuroinflammation, and calcium homeostasis, thereby determining RGC fate. Post-translational modifications such as phosphorylation, acetylation, and ubiquitination can influence intracellular signaling pathways, gene expression and cellular stress responses by regulating the function, stability, and interaction of proteins within retinal cells, thereby shaping retinal cellular responses to injury and stress. This article comprehensively summarizes the effects of mitochondrial quality control and post-translational modification on retinal ganglion cells after retinal ischemia–reperfusion, explores the influence of post-translational modification on the above process, and discusses the potential of traditional Chinese medicine monomers in protecting retinal ganglion cells.