Kyushu team traces glaucoma’s nighttime pressure rise in mice

At night, pressure inside the eye rises—and a daytime appointment may not catch it. Researchers at Kyushu University have traced that rise to a molecular chain involving norepinephrine and RHOB, identifying a possible new route for detecting and controlling one of glaucoma’s main risk factors. The study used human cells and mice, not patients.

The team focused on the trabecular meshwork, the eye’s fluid-drainage tissue. Its cells do more than let fluid pass: they also take up and remove small particles and waste that could obstruct the pathway. When exposed to norepinephrine, human and mouse cells changed their genetic activity; 18 genes increased in both systems, leading the researchers to RHOB, a molecule involved in cell shape, movement and internal transport.

The experiments connected RHOB to the loss of that cleaning function. Removing RHOB from human trabecular meshwork cells increased their ability to take up and clear particles. Raising RHOB had the opposite effect, reducing cleaning activity and fluid movement. In mice, eye drops that inhibited the RHO-ROCK pathway controlling RHOB reduced the nighttime rise in intraocular pressure.

So what changes in practice? Not yet a prescription. But the pathway gives researchers a target for treatments designed around the eye’s daily rhythm, and it could encourage glaucoma monitoring that looks beyond a single daytime pressure reading. That matters because glaucoma damages the optic nerve progressively and vision loss develops slowly, making early detection important.

The Kyushu team, led by Associate Professor Keisuke Ikegami, says the findings are not intended for immediate clinical application. ROCK inhibitors are already used in glaucoma treatment, but further work is needed to determine the most effective time for administration and how these drugs alter the pressure rhythm. The results were published in Communications Biology in 2026.