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Study targets key molecule to reverse kidney damage in mice
Date:3/7/2012

eptor, the molecule suppressed inflammation, cell death and fibrosis formation, as well as reversing established fibrosis and allowing kidneys to regenerate functional cells, he adds.

Further experiments showed that the test drug worked even better in the mice when given in combination with ACE inhibitors, the anti-hypertensive drugs now considered a standard therapy for chronic kidney disease which work by targeting another molecular process.

"Targeting the receptor not only stops fibrosis, it removes established fibrosis, and it works in combination with an existing drug used in patients," Kalluri notes. "The next step is to test this molecule in the clinic."

The mice studies are "a good first step," said Al-Awqati. "It will be interesting to pin down the role of the BMP-7 pathway in kidney fibrosis in people."

Going forward, Kalluri's group will continue to study these molecular players and their roles in fibrosis in other organs, including the liver, lung, intestine and heart in the hopes of expanding the experimental-drug pipeline. "If you don't have a pipeline of experimental drugs, how will you succeed in coming up with new drugs?" he asks.


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Contact: Bonnie Prescott
bprescot@bidmc.harvard.edu
617-667-7306
Beth Israel Deaconess Medical Center
Source:Eurekalert

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