Abstract
Glaucoma is the most substantial cause of irreversible blinding, which is accompanied by progressive retinal ganglion cell damage. Retinal ganglion cells are energy-intensive neurons that connect the brain and retina, and depend on mitochondrial homeostasis to transduce visual information through the brain. As cofactors that regulate many metabolic signals, iron and zinc have attracted increasing attention in studies on neurons and neurodegenerative diseases. Here, we summarize the research connecting iron, zinc, neuronal mitochondria, and glaucomatous injury, with the aim of updating and expanding the current view of how retinal ganglion cells degenerate in glaucoma, which can reveal novel potential targets for neuroprotection.
Highlights
Glaucoma involves irreversible optic nerve injury, which remains an urgent clinical challenge affecting 3–4% of people over 40 years of age; the global prevalence of glaucoma is expected to escalate to approximately 112 million people by 2040 (Tham et al, 2014)
Specifying how metal ions influence the mitochondria might provide much needed insight into the bottleneck of glaucoma. This is an exciting time for research in glaucoma mitochondrial biology, with the emergence of several intriguing findings regarding mitochondrial biogenesis, dynamics, and quality control
retinal ganglion cells (RGCs) are extremely dependent on mitochondria, and the function of mitochondria in glaucoma patients is of particular interest
Summary
Glaucoma involves irreversible optic nerve injury, which remains an urgent clinical challenge affecting 3–4% of people over 40 years of age; the global prevalence of glaucoma is expected to escalate to approximately 112 million people by 2040 (Tham et al, 2014). With a greater understanding of the relationships among glaucoma, iron, and zinc, it is important to further elucidate the mechanism of metal dyshomeostasis in RGCs and the subsequent cellular pathophysiological signaling processes.
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