A Protein Called Adam17 May Play a Role in Diabetic Kidney Disease—New Research Points to a Potential Target

Type 1 diabetes can damage the kidneys over time, a condition called diabetic kidney disease (DKD). The damage happens through multiple pathways: high blood sugar creates metabolic stress, the immune system becomes overactive, cells send distress signals, and scarring builds up in kidney tissue. Understanding which proteins drive these processes could eventually lead to new protective strategies.

One protein that scientists have begun investigating is called Adam17. Earlier studies suggested that removing Adam17 from specific cell types might protect kidneys, but researchers wanted to know what happens when the entire body lacks this protein during diabetes.

Scientists induced type 1 diabetes in laboratory mice and then removed Adam17 throughout their bodies using a genetic technique. They then measured kidney function, structural damage, immune activity, cellular stress signals, and scarring.

The results showed that mice without Adam17 preserved their glomerular filtration rate—a key measure of how well kidneys filter waste—even as their blood sugar remained high. These mice also had less kidney tissue damage, fewer immune cells infiltrating the kidney, lower levels of inflammatory chemicals, and significantly reduced scarring compared to control diabetic mice.

Surprisingly, the kidney protection occurred despite these mice still having protein in their urine, suggesting that Adam17 affects kidney damage through mechanisms beyond just controlling glomerular permeability. At the molecular level, Adam17-deficient mice showed reduced activation of certain stress-response pathways while maintaining others, pointing to selective rather than blanket changes in how kidney cells respond to diabetes.

This research identifies Adam17 as a potential target for slowing kidney disease progression in type 1 diabetes. The fact that kidney function improved even with persistent high blood sugar suggests that strategies targeting Adam17 could work alongside, rather than instead of, blood sugar management.

However, this work was conducted in mice with experimentally induced diabetes. Human kidneys are far more complex, and responses to Adam17 removal might differ. The study does not tell us whether blocking Adam17 would be safe or effective in people, nor does it suggest any current treatment. Much additional research—including studies in other animal models and eventually clinical trials—would be necessary before any therapeutic approach could be considered.

Diabetic kidney disease is a serious long-term complication of type 1 diabetes, and current treatments for kidney protection are limited. Identifying new proteins and pathways involved in kidney damage creates a larger toolkit for researchers developing future therapies.

Studies like this one contribute to the broader effort to understand type 1 diabetes complications at a deeper level. By mapping how different proteins and cellular processes interact during kidney disease, scientists can design more targeted and potentially more effective interventions to preserve kidney function and quality of life.

Source: International journal of molecular sciences. Evidence type: PubMed indexed literature. Type1Cure is an information and intelligence hub, not a medical advice service. This article summarizes published research and does not provide diagnosis, treatment, or personal medical guidance. Always talk to your own care team before changing anything about your Type 1 diabetes management.