“We also showed that anti-IL-11 therapy can treat kidney failure, reverse established chronic kidney disease, and restore kidney function by promoting regeneration in mice while being safe for long-term use.”
The researchers came to this discovery by showing that renal tubular cells release IL-11 following kidney damage. Renal tubular cells line the tiny tubes located inside the kidneys.
Then, following the IL-11 release, a cascade effect is signaled and causes the increased expression of a gene known as Snail Family Transcriptional Repressor 1 (SNAI1). This gene disrupts cell growth and leads to kidney dysfunction.
So, the researchers administered an antibody that binds to IL-11 in order to turn off the cascade process. They found that the antibody prompted the proliferation of kidney tubule cells and led to a reversal of inflammation and fibrosis.
In other words, the injured kidneys in the preclinical model of human diabetic kidney disease regenerated, and renal function was restored.
Past clinical trials, which used an antibody that binds to a different pro-fibrotic molecule known as transforming growth beta, had been unsuccessful. However, this novel approach has reinstated optimism among the research team.
“By boosting the kidney’s intrinsic capability to regenerate, Cook and Widjaja have shown that we can restore function to a damaged kidney,” Coffman said.
“This discovery could be a real game-changer in the treatment of chronic kidney disease– which is a major public health concern in Singapore and globally– bringing us one step closer to delivering the benefits promised by regenerative medicine.”
To read the study’s complete findings, visit the link here.
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