UCLA ‌Research Identifies Key Role in Kidney Scarring

​ ⁤ Updated June 17, 2025

Los‍ angeles — A⁣ new study ‌from UCLA has revealed a critical factor in determining the extent of kidney scarring following injury. The research, utilizing ⁢mouse models and ⁢human genetic ⁤data, points to a potential ⁣precision ⁢medicine approach to halt the progression of chronic​ kidney ‌disease.

Published in science Translational ⁣Medicine, the study highlights the notable role of type 5 collagen in kidney‍ fibrosis. Researchers found that an‍ experimental therapy could prevent kidney‍ failure⁣ in ‍individuals with a high risk of developing the condition. The study emphasizes the importance​ of understanding the role of⁣ type 5 collagen in kidney health.

Chronic kidney disease, affecting more than one in seven adults in the U.S. and 800 million people globally, results from conditions ⁤like diabetes and ​high blood⁣ pressure. As‌ the disease ⁣progresses, excessive scar tissue buildup impairs the kidneys’ ability to filter toxins, often leading⁣ to kidney failure. Currently, no therapies directly target or reverse this process, leaving patients dependent on ‌dialysis or transplants.

Dr.​ Arjun Deb, the study’s senior author at UCLA’s Broad Center⁤ of Regenerative Medicine, saeid scarring is a ​strong predictor of kidney ⁢failure. He added that the research indicates that differences in type 5‌ collagen expression explain variations⁤ in scarring. Testing‌ for this gene or protein could identify those at greater risk.

Earlier research by Deb​ on ‌heart injuries⁢ showed that mice lacking type ‍5 collagen production experienced more extensive scarring after heart attacks.

To ​see if similar mechanisms applied to kidney injury, the team analyzed data from the UK Biobank, a⁤ long-term study tracking over 1.5 million people. They discovered that expression of Col5a1, ⁤the gene‌ encoding type 5 collagen, strongly correlated with the ‍risk of ⁣developing chronic kidney disease over a decade.

According to Deb,Col5a1 expression could serve as a biomarker to identify individuals likely to‌ progress to kidney failure.

Experiments with mice confirmed these findings. Mice⁣ with low Col5a1 ‍developed ‍more severe fibrosis and ‍progressed more rapidly to kidney failure after injury. Type 5 collagen plays ⁤a crucial role in maintaining‌ the structure of‍ scar tissue, acting like threads holding fabric together, Deb explained.

“Collagens are fibrillar in⁤ nature, and they give strength ⁢to scar tissue,” Deb said. “The ⁢way the fibers are‍ arranged is ‍very critically important. Type 5 collagen ensures the fabric of a scar is ‍not woven haphazardly — that it is⁤ instead structured and stable.”

Without type 5 collagen, the body perceives scar tissue as weaker, activating αvβ3 integrins. These receptors in fibroblast cells⁣ respond by producing even more scar tissue,‌ worsening ⁢kidney function and leading to failure.

The ‍team then explored blocking integrin activity using Cilengitide, a drug initially developed as an anti-cancer therapy. While safe, it proved ineffective against cancer ‌in clinical trials.Though, treating animals with decreased type 5 collagen‍ with Cilengitide substantially reduced‌ kidney fibrosis and ‍slowed disease progression.‌ It had no effect on mice with normal ‍Col5a1​ expression, highlighting its‍ potential as a targeted therapy.

Deb noted the⁣ exciting ⁤opportunity to repurpose this FDA-deemed-safe drug for a different indication.

What’s next

Deb’s team​ is now working to develop a blood test⁤ to measure Col5a1 levels in patients with chronic ‌kidney disease. If⁤ validated,this biomarker could guide treatment decisions,identifying patients who‍ could benefit ​from this targeted approach to slowing disease progression. ⁣Researchers are also investigating if these mechanisms contribute to fibrosis in the liver and blood ‍vessels.