Pathophysiology of intraocular haemorrhage: Role of iron in cell death

Abstract

AbstractRetinal haemorrhages are present in several retinal pathologies, such as exudative AMD, diabetic retinopathy, or myopic degeneration. As a consequence of erythrocytes lysis following haemorrhage, haemoglobin (Hb) is released into the extracellular space, and heme is degraded into iron, which becomes under a free (unbound) form. While iron is essential for retinal functions, labile free iron enhances Fenton reaction and therefore leads to oxidative stress. Cones are the most sensitive retinal cells to iron excess and local accumulation of iron rapidly induces photoreceptors and retinal pigment epithelium cells death. A local retinal homeostasis of iron exists to equilibrate iron level in retinal cells, but a deficiency of iron‐related proteins causes iron accumulation and retinal degeneration. Heme‐binding proteins, hemopexin and haptoglobin, and their receptors, as well as heme transporters were also found expressed in retinal cells suggesting their roles in retinal iron regulation. As therapeutic strategy, chemical chelators used to control iron accumulation in systemic iron overload diseases, have demonstrated efficiency to protects the retina in various models of retinal degenerations. Our team uses transferrin (TF), the iron transporter protein, to reduce iron overload and therefore preserve visual function. Control of iron impairment in retinal tissues may be a therapeutic strategy during haemorrhages.