Researcher are studying a mouse-based model to find how excessive tissue scarring, known as interstitial fibrosis, is partially responsible for an increase in chronic kidney disease in the U.S.
Dr. Raymond Harris of Vanderbilt University and others earlier had theorized that a protein called epidermal growth factor receptor (EGFR) may play a role in the development of diabetic nephropathy and kidney fibrosis, but without certainty of EGFR’s role in a kidney area called the renal tubule, a Vanderbilt release said.
Subsequently the researchers discovered that mice with tubulointerstitial fibrosis experienced abatement of symptoms with genetic or pharmacologic manipulation of EGFR activity, the release said. Results were published recently in the FASEB Journal, a biology journal published by the Federation of American Societies for Experimental Biology.
The Vanderbilt team concluded that the mouse model offers a way to identify and target treatment modes for fibrosis, the release said. Harris and his colleagues were able to perform the study with help from grants allotted by the National Institutes of Health.
