Abstract
Iron plays an important role in a wide range of metabolic pathways that are important for neuronal health. Excessive levels of iron, however, can promote toxicity and cell death. An example of an iron overload disorder is hemochromatosis (HH) which is a genetic disorder of iron metabolism in which the body’s ability to regulate iron absorption is altered, resulting in iron build-up and injury in several organs. The retina was traditionally assumed to be protected from high levels of systemic iron overload by the blood-retina barrier. However, recent data shows that expression of genes that are associated with HH can disrupt retinal iron metabolism. Thus, the effects of iron overload on the retina have become an area of research interest, as excessively high levels of iron are implicated in several retinal disorders, most notably age–related macular degeneration. This review is an effort to highlight risk factors for excessive levels of systemic iron build-up in the retina and its potential impact on the eye health. Information is integrated across clinical and preclinical animal studies to provide insights into the effects of systemic iron loading on the retina.
Highlights
Iron is essential for neuronal development and function (Lozoff et al, 2003)
Current animal studies indicate that the major driving factor in retinal degeneration may be iron overload as opposed to the genetic mutation itself having a direct effect, even though many hemochromatosis molecules have been found in the retina (Gnana-Prakasam et al, 2009a)
Iron is known to play a critical role in the metabolic activities of the retina the RPE and photoreceptors, and the inner retina
Summary
Iron is essential for neuronal development and function (Lozoff et al, 2003). Iron plays key roles in neuronal metabolism, oxygen transport, oxidative phosphorylation, myelin production, and the synthesis of neurotransmitters, as reviewed in detail elsewhere (Crichton et al, 2011; Ward et al, 2014). High intracellular iron levels can affect the expression of several classes of genes including iron-dependent oxidative metabolism and the attendant oxidative stress genes (Casey et al, 1988; Ingrassia et al, 2019) Another suggested pathway through which errors in iron metabolism can be deleterious is ferroptosis, a recently identified form of cell death, which has been implicated in a number of central nervous system (CNS) diseases (Dixon et al, 2012; Guiney et al, 2017; Lane et al, 2018; Moreau et al, 2018; Masaldan et al, 2019). We mainly focus on retinal structural and functional changes in clinical cases and preclinical models This is important because currently there is no routine clinical visual check–up for high-risk demographic such as patients with hemochromatosis or even people with high levels of dietary iron intake which may have been at risk of retinal iron accumulation and disease-related sequelae.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
