Prerana Sharma is a postdoctoral researcher at the University of South Florida. She investigates the molecular mechanisms governing corneal inflammation and tissue homeostasis to prevent scarring and vision loss. In this Postdoc Portrait interview, she shares what initially drew her to the field and discusses the importance of her work.
Elucidating Signaling Pathways in Corneal Tissue
Q | What drew you to studying corneal disease?
I was drawn to this field during my PhD at the L. V. Prasad Eye Institute (LVPEI), a globally recognized center that integrates research with patient-centered care. Although my work was primarily in a basic science setting, I was constantly exposed to a research environment where clinical relevance was central. LVPEI’s model emphasizes translational research aimed at addressing real-world causes of vision loss, particularly in underserved populations.
What influenced me most was seeing how fundamental discoveries in the lab were closely aligned with clinical challenges, such as corneal blindness and inflammation-driven pathology. Even without direct patient interaction, it was clear that unmet clinical needs shaped the questions we pursued. In a setting where preventable blindness remains a significant burden, this strong connection between bench research and patient impact motivated me to focus on understanding the molecular mechanisms of corneal disease. My goal is to contribute foundational insights that can ultimately inform the development of effective, accessible therapies.
Q | What scientific problem are you trying to solve?
Corneal opacity is a leading cause of blindness in the industrialized world, primarily resulting from disrupted corneal transparency. Under normal conditions, the cornea maintains a stable, transparent state through tightly regulated interactions between corneal nerves and resident cell populations that preserve tissue homeostasis. However, local injury, systemic disease, or infection can disturb this balance, triggering inflammatory responses. When inflammation is prolonged or inadequately controlled, it can lead to structural damage, scarring, and ultimately loss of vision.
My research focuses on elucidating the molecular mechanisms that govern corneal inflammation and its resolution. By identifying key signaling pathways and cellular interactions involved in this process, I aim to uncover novel therapeutic targets. These insights could enable the development of more effective interventions to prevent or mitigate inflammation-induced corneal opacity and preserve visual function.
Q | What’s one thing you learned from your research that you didn’t expect?
One thing I did not expect when I began working in this field was how central corneal research is to both vision science and broader biomedical questions. I initially viewed eye research as relatively specialized, but I came to appreciate that the cornea is a powerful model for studying inflammation, nerve-immune interactions, wound healing, and tissue regeneration.
I was also surprised by the breadth of basic science approaches required to address these questions. Investigating corneal inflammation demanded integrating molecular biology, imaging, cell culture systems, and in vivo models to capture both mechanistic detail and physiological relevance. Working in a translational environment further reinforced how closely these techniques are tied to clinically meaningful outcomes.
This experience reshaped my perspective: impactful research often requires crossing traditional disciplinary boundaries. It highlighted that even a seemingly niche field can offer deep insights into fundamental biological processes while maintaining a clear path toward therapeutic application.
Working Toward Blindness Therapeutics
Q | If your research succeeds, what are the long-term implications?
This work could help shift how we approach corneal disease, moving from managing symptoms to preventing damage at the molecular level. Instead of relying mainly on treatments like long-term anti-inflammatory drugs or corneal transplants, we could develop more targeted therapies that stop inflammation before it leads to scarring and vision loss. On a broader level, preserving vision has a direct impact on quality of life. People can remain independent, continue working, and stay connected to their communities. This is especially important in regions where access to advanced surgical care is limited. From a scientific perspective, understanding how inflammation is regulated in the cornea could also inform research in other tissues, since many of the same biological pathways are involved. So, while the focus is on the eye, the implications could extend well beyond it.
Q | What question are you most excited to answer next?
The question I am most excited to answer next is how corneal inflammation resolves at the molecular level, not just how it starts. While a lot is known about the triggers of inflammation, the mechanisms that actively restore homeostasis are still not well understood. I am particularly interested in identifying the key signaling pathways and cell-cell interactions that drive resolution rather than chronic damage. Understanding this could open the door to therapies that promote healing instead of simply suppressing inflammation. It would allow us to design interventions that preserve corneal transparency more effectively and reduce the risk of scarring. More broadly, uncovering these mechanisms could provide insights into how other tissues recover from inflammation, making this question both clinically relevant and biologically fundamental.
Responses have been edited for length and clarity.
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