Gopi Sundaramoorthy is a postdoctoral researcher at the University of South Florida. He develops neuroprotective therapies to prevent retinal pigment epithelium degeneration in age-related macular degeneration. In this Postdoc Portrait interview, he shares how he intends to provide better treatments in a field with limited effective options.
Uncovering Pathways in Retinal Degeneration
Q | What drew you to studying retinal degeneration?
I was drawn to retinal degeneration research because of the major unmet clinical need in age-related macular degeneration (AMD), particularly the dry form of the disease, which currently lacks effective treatments. Vision loss from AMD has a profound impact on quality of life, independence, and aging populations worldwide, making it both a scientifically important and personally motivating area of study. I became especially interested in the retinal pigment epithelium (RPE) because these cells play a central role in maintaining retinal health, yet they are highly vulnerable to oxidative stress, inflammation, and metabolic dysfunction.
My interest further developed through working with molecular and transcriptomic approaches to study how protective pathways can be activated in stressed RPE cells. I am motivated by the possibility of identifying mechanisms that not only explain disease progression but also lead to therapies capable of preserving vision and improving patient outcomes.
Q | What scientific problem are you trying to solve?
I am working to address the problem of RPE degeneration in AMD, a leading cause of irreversible vision loss worldwide. In AMD, oxidative stress, mitochondrial dysfunction, inflammation, and ferroptotic cell death progressively damage RPE cells, which are essential for maintaining photoreceptor survival and retinal health. Current treatments are limited, especially for the dry form of AMD, where there are no widely effective therapies to halt disease progression.
My research focuses on identifying protective mechanisms that can improve RPE survival under oxidative stress conditions. Specifically, I study the therapeutic potential of EPO-R76E, a modified erythropoietin variant with tissue-protective but reduced erythropoietic activity, as well as nanoparticle-based delivery strategies to enhance cellular protection. Using RNA sequencing and molecular analyses, I investigate pathways involved in oxidative stress responses, ferroptosis, inflammation, and metabolic regulation in RPE cells and mouse models. The long-term goal is to develop safer and more effective neuroprotective therapies that preserve retinal function and prevent vision loss in AMD patients.
Developing Protective Therapies for Age-Related Macular Degeneration
Q | What’s one thing you learned from your research that you didn’t expect?
One unexpected finding from my research was how interconnected oxidative stress, inflammation, and ferroptosis are in RPE degeneration. Initially, I expected oxidative stress to act mainly as a direct source of cellular damage. However, through transcriptomic and molecular analyses, I found that oxidative stress can trigger broad changes in metabolic and inflammatory signaling pathways that amplify cell vulnerability in ways that are not immediately obvious. In particular, I was surprised by how strongly ferroptosis-related pathways were linked to mitochondrial dysfunction and lipid metabolism in stressed RPE cells.
Another unexpected insight was the extent to which protective interventions, such as EPO-R76E expression or nanoparticle-based treatments, influenced multiple cellular pathways simultaneously rather than targeting only a single mechanism. Instead of acting through one isolated effect, these approaches appeared to reshape broader stress-response networks involved in survival, inflammation, and antioxidant defense. This reinforced the importance of studying retinal degeneration as a complex systems-level process rather than focusing on a single pathway alone.
Q | If your research succeeds, what could it change for science or society?
It could help develop new treatments for dry AMD by protecting retinal cells from oxidative stress and degeneration. This could preserve vision, improve quality of life for patients, and provide insights into other age-related neurodegenerative diseases.
Q | What question are you most excited to answer next?
I am most excited to understand how protective pathways can be activated in the long term in RPE cells to prevent degeneration without causing unwanted side effects. I am particularly interested in identifying how therapies such as EPO-R76E or nanoparticle-based approaches regulate oxidative stress, ferroptosis, and inflammation together to preserve retinal function in patients with AMD.
Responses have been edited for length and clarity.
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