ARVO 2026: Retinal neuroprotective role of Cav1

In this brief research spotlight, Olawale Bankole, a graduate student in the Department of Biochemistry and Physiology at the University of Oklahoma Health Sciences Center, discusses his work on retinal inflammation and neuroprotection. He focuses on major blinding diseases such as glaucoma, age-related macular degeneration (AMD), and diabetic retinopathy, all of which are strongly driven by chronic inflammation in the retina. Bankole explains that while inflammatory responses are initially protective, uncontrolled or excessive inflammation becomes detrimental and accelerates disease progression.

His research centers on caveolin‑1, a membrane-associated protein expressed in many cell types that plays a key role in modulating inflammatory signaling. In the retina, Müller glial cells show unusually high levels of caveolin‑1, but in a non‑canonical configuration. Bankole’s group discovered that this is linked to the absence of a “sibling” structural protein, cavin‑1/PTRF, which is normally required to form proper caveolae domains in the plasma membrane.

By reintroducing cavin‑1 into these cells, the team can sequester caveolin‑1 into its appropriate membrane microdomains, thereby reducing its pro‑inflammatory activity. This strategy does not target a single receptor or pathway; instead, it acts at the level of the caveolar membrane platform that organizes multiple innate immune receptors. As a result, their approach is immune receptor–agnostic, enabling simultaneous down‑regulation of several inflammatory pathways at once. Bankole’s work highlights a promising avenue for broadly dampening retinal inflammation and potentially slowing the progression of multiple retinal degenerative diseases.