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Editors Selection IGR 17-3

Basic Science: IOP and Iron Homeostasis

Comment by Shan Lin on:

104855 Pathologically high intraocular pressure disturbs normal iron homeostasis and leads to retinal ganglion cell ferroptosis in glaucoma, Yao F; Peng J; Zhang E et al., Cell Death and Differentiation, 2023; 30: 69-81

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This study from Yao et al. examined the role of iron homeostasis in retinal ganglion cell injury secondary to pathologically high intraocular pressure (IOP). There have been previous population studies which showed that serum iron levels (in the form of ferritin) and excessive iron supplementation are correlated with glaucoma diagnosis.^1,2 The authors used in vitro, animal, and human models to assess whether ferroptosis (a form of iron-related cell apoptosis) plays a role in glaucoma. The in vitro model utilized the immortalized retinal cell line R28, a retinal precursor line from rat retinas. Oxygen deprivation (and subsequent reoxygenation) was used to simulate injury to these cells. The animal model for glaucoma consisted of male C57BL/6 mice which received cannulation of their anterior chambers and elevation of their IOP to 120 mmHg for 90 minutes. The human model included the assessment of blood serum from inpatients who had acute primary angle closure glaucoma (APACG). Compared to controls, there was elevated total serum iron and ferric iron. In the in-vitro model, oxygen deprivation led to accumulation of ferrous iron as well as alterations in the expression of genes related to iron metabolism. In the animal model, there was also abnormal accumulation of iron and alterations in related cellular factors supporting the role of ferroptosis in optic nerve damage. Moreover, the use of deferiprone (iron-chelating agent) attenuated some of the pressure-induced damage to the ganglion cell complex and the retinal ganglion cells in the mouse model. In summary, the present studies support a possible association of high-IOP related injury to the eye with iron metabolism and iron-related apoptotic events. The evidence is strong, although does not necessarily prove a pathophysiological role for iron. Future studies can help discern causal links and perhaps provide a mechanism by which cellular damage and death can be prevented with iron-blocking agents.

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