In a study in mice, the scientists found that healing in the kidneys and hearts was driven by a protein called Indian Hedgehog (IHH), which is produced and released by a subset of cells in aged and injured kidneys.
Experts say more studies are needed to explore IHH as a potential target for therapies to treat chronic kidney disease (CKD), a condition that affects 10 percent of the world’s population.
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CKD is a term used to cover any form of kidney disease that continues for more than a few months.
It can affect people of any age, but older people are more likely to experience some level of CKD.
Although CKD primarily causes kidney damage, it is also a major risk factor for accelerated cardiovascular disease and premature death.
Progressive fibrosis (scarring of the kidneys) is a common feature of all CKD, but the mechanism underlying this connection is not fully understood.
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Research by scientists at the University of Edinburgh has now identified a subset of epithelial cells, cells that make up body tissue, that produce IHH and are only present in the kidneys of aged or injured mice.
They showed that these cells produced IHH in response to the activation of another protein called TNF, which is well known as a driver of inflammation.
By blocking the actions of TNF or IHH in mouse models of kidney scarring, the team found that scarring in the kidney was reduced and kidney function was also better preserved.
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Increased levels of scarring in the heart also returned to normal levels.
In humans, the team showed that circulating IHH levels were significantly elevated in CKD patients.
Patients with cardiovascular disease also had higher levels of IHH than those without heart problems.
The findings offer hope that blocking the TNF/IHH signaling pathway could ameliorate renal and cardiac fibrosis problems, the leading cause of morbidity and mortality in CKD patients.
Dr David Ferenbach, an expert in renal medicine at the University of Edinburgh and lead author of the study, said: “There is a great unmet need for better treatments to stop the progressive kidney scarring and cardiovascular problems that plague so many CKD patients.
“I am excited about the potential of this work and the new insights that will be gained about the role of IHH as a major driver of multi-organ fibrosis, which we hope can be a first step on the path to better treatments for patients.”
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The study, published in the journal Science Translational Medicine, was funded by Kidney Research UK, the Wellcome Trust and the Medical Research Council UK.