Researchers at the University of Virginia have identified a previously unrecognized factor that contributes to age related macular degeneration and other common eye conditions that can lead to vision loss. The discovery centers on the metabolism related FTO protein, which appears to influence the growth of abnormal blood vessels in the eye. When the FTO protein is blocked, the pathological vessel growth can be halted, offering a potential new approach to protecting sight. The team has shared these findings in Signal Transmission and Targeted Therapy, marking a step forward in understanding how metabolism intersects with eye health.
The macula lies at the center of the retina and consists of a specialized network of cells that are essential for detailed central vision. Above the underlying retinal pigment epithelium and separated from the vascular system by a thin membrane, this region is particularly sensitive to age related changes. As people grow older, abnormal blood vessels may begin to form and expand in this area. These vessels often originate from the interface known as Bruch’s membrane, and their growth can damage delicate nerve fibers that support clear, sharp vision. The result can be a measurable decline in visual quality and daily functioning for many individuals.
It is well established that excessive VEGF protein drives unwanted vascular growth in the eye, a process that fuels the progression of degenerative changes. Treatments currently available for these conditions can slow progression and improve vision for some, but their benefits are typically temporary and may require ongoing administration. This reality underscores the need for new strategies that address the root triggers of abnormal vessel formation rather than merely mitigating symptoms.
In the recent study, researchers demonstrated that the FTO protein, which is linked to cellular metabolism, also plays a significant role in the sprouting of ocular vessels. The work indicates that FTO influences the level of VEGF in eye tissues, thereby modulating the extent of abnormal vascular growth. Importantly, experiments conducted in laboratory mice showed that inhibiting the FTO protein led to a meaningful decrease in VEGF without producing adverse side effects. These results point to the FTO pathway as a promising target for preventing or slowing the visual damage associated with AMD and related conditions.
Beyond the immediate implications for treatment development, the study provides a framework for future research into how metabolic regulators interact with eye anatomy to influence disease processes. By linking metabolism to vascular dynamics in the retina, scientists can pursue new approaches that complement existing anti-VEGF therapies and explore combination strategies that may yield longer lasting benefits for patients. The implications extend to broader questions about how metabolic factors shape the health of neural tissues and supporting structures throughout the eye. These findings open avenues for exploring preventive strategies that could preserve vision in aging populations. [Attribution: University of Virginia research team, study on FTO and AMD]