Scientific breakthrough paves way for potential cure for diabetes complications

Researchers from the University at Albany and New York University Grossman School of Medicine have discovered way to block a key cellular pathway that drives chronic inflammation and impairs wound healing in people with diabetes.

The breakthrough could offer a new therapeutic option for stopping the harmful effects of both type 1 and type 2 diabetes at the source.

In their latest work, the researchers identified and developed a small-molecule drug capable of disrupting an intracellular chain reaction known to contribute significantly to diabetes-related complications.

“Current treatments for diabetes primarily focus on slowing disease progression; however, they do not address the underlying inflammation that contributes to the complications of diabetes. Our findings point to a promising new pathway for treating diabetes in the future,” said Alexander Shekhtman, co-senior author, Professor at the Department of Chemistry and the RNA Institute, Albany.

He added that the results pave the way for developing therapies for both types of diabetes, as well as for for designing markers that can measure how well the new treatment works in live animals.

In people with diabetes, a type of harmful molecule known as "advanced glycation end products (AGEs)" accumulate in tissues throughout the body. These molecules activate a cell surface sensor known as the “Receptor for Advanced Glycation End products (RAGE)”, which in turn triggers a molecular structure inside cells called "Diaphanous-1" (DIAPH1).

Typically, DIAPH1 supports normal cell functions, but when overstimulated, it leads to chronic inflammation, contributing to cardiovascular disease and delayed wound healing.

Using structural biology techniques, the research team built a model to understand how the RAGE receptor activates DIAPH1. This allowed them to pinpoint a binding site on DIAPH1 that facilitates the pathway.

WAM