"This is very exciting," Mohr said. "We know that we can't regulate production of GAPDH because it's necessary for producing energy throughout the body. But since siah-1 is produced only when glucose levels are high, regulating it doesn't cause any problems. If we can figure out how to stop siah-1 production, it may lead to new treatments for diabetic retinopathy."

Mohr explained that stopping GAPDH from moving into M-ller cell nuclei is important to halting the progress of diabetic retinopathy. Even after glucose levels are lowered and stabilized in diabetics, GAPDH continues to accumulate in M-ller cell nuclei. So the retinal damage keeps worsening, just more slowly.

"If we can keep GAPDH out of the nuclei, we may be able to completely stop diabetic retinopathy," Mohr said. "Our next step is to figure out if both the GAPHD and the siah-1 proteins have to be together in a complex to cause cell death."

Source: Michigan State University