Researchers find key protein that influences kidney scarring and disease progression.
Scientists at UCLA have been digging into why some people with kidney problems end up with more scarring than others. Scarring in the kidneys is serious—it can make the organs stop working properly over time. The team looked at both lab mice and data from people and found something interesting: a protein called type 5 collagen seems to play a big part in how much scarring happens after the kidneys are hurt. While it’s not one of the main parts of scar tissue, it has an important job in how the scars form and hold together. If this protein is missing or low, the body tends to build messy, disorganized scar tissue that causes more damage. That extra damage makes kidney disease worse and can lead to kidney failure, meaning the person would eventually need dialysis or even a transplant.
One of the lead researchers, Dr. Arjun Deb, had already studied this type of collagen in heart injuries. In that earlier work, he found that mice without the ability to make type 5 collagen developed worse heart scarring after a heart attack. So, the team decided to see if the same thing happened in the kidneys. They pulled together information from a big health database called the UK Biobank, which tracks over a million people over time. The data showed that people with lower levels of the gene that makes this collagen were more likely to get kidney disease later in life. That made them think this protein could help doctors predict who might be at higher risk.
To test it further, they ran experiments on mice with and without the ability to make type 5 collagen. The results matched what they’d seen in people. Mice with lower levels of the protein had more scarring and got sicker faster after their kidneys were injured. When type 5 collagen is missing, scar tissue forms in a weaker and more chaotic way. That sets off a response in cells called fibroblasts. These cells try to fix the damage by making even more scar tissue, but they overdo it. The researchers described it like trying to patch a hole in a wall with too much glue—eventually, the fix causes more harm than good.
After spotting this cycle, the team searched for a way to stop it. They focused on a part of the fibroblast cell that reacts when it senses messy scar tissue. That part is called integrin αvβ3. They found a drug, Cilengitide, that was made years ago for cancer but didn’t work out for that purpose. Interestingly, it turned out to be helpful here. When given to the mice missing type 5 collagen, the drug slowed down the scarring and helped protect their kidneys. But in mice with normal levels of the collagen, the drug didn’t do anything. That means it might work best for people who are especially at risk, not for everyone.
Now, the team wants to develop a blood test that could show how much of the type 5 collagen a person makes. If it works, doctors could use it to spot who’s more likely to have fast-moving kidney disease and offer them more targeted help. The researchers are also wondering if this scarring problem shows up in other parts of the body, like the liver or blood vessels, and whether this same drug could help there too.
The drug hasn’t been approved for treating scarring yet, but the idea is promising. The hope is that one day, people who are likely to develop serious kidney problems could get tested early and possibly take medicine that slows the damage. That could keep them healthier longer and maybe even avoid needing dialysis or a new kidney altogether.
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