In A Novel Preclinical Study, Researchers Have Discovered How To Restore Damaged Kidney Function By “Boosting” The Organ’s Intrinsic Capability To Regenerate

In the United States, the average wait time for a kidney transplant is between three and five years. And according to the American Kidney Fund, there are 92,000 people currently awaiting the organ– accounting for 87% of the national transplant waiting list.
But, in a remarkable new study, researchers from Duke-NUS Medical School and the National Heart Center Singapore (NHCS) have found that restoring impaired kidney function via regenerative therapy may be possible.
During a preclinical study, which has since been published in Nature Communications, the team discovered that blocking IL-11– a damaging, scar-regulating protein– enabled damaged kidney cells to regenerate. This ultimately restored kidney function that was impaired by acute injuries and disease.
“Kidney failure is a global epidemic. Closer to home, Singapore ranks first in the world for diabetes-induced kidney failure and fourth in terms of kidney failure prevalence. The contribution of chronic kidney disease to mortality is rapidly increasing, suggesting there are shortcomings in current therapeutic approaches,” explained Anissa Widjaja, an assistant professor, and molecular biologist at Duke-NUS.
Widjaja ultimately joined forces with Stuart Cook, the head of Cardiovascular Genetics and Genomics at the National Heart and Lung Institute (NHLI) in London, as well as world-leading nephrologist Thomas Coffman and colleagues in Germany.
Then, the team began to investigate IL-11, a protein that triggers scarring in organs– such as the lungs, liver, and heart– in chronic and acute kidney disease.
The researchers’ findings suggest that IL-11 triggers a domino effect of molecular processes– leading to fibrosis (scarring), inflammation, and loss of function.
Conversely, the team also discovered that kidney damage could be prevented and even reversed by using a neutralizing antibody to inhibit IL-11.
“We found that IL-11 is detrimental to kidney function and triggers the development of chronic kidney disease,” Cook detailed.

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“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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