Researchers lead by Li Yang, MD, in the laboratory of Dr. Joseph Bonventre, chief of the Renal Division at the Brigham and Women’s Hospital and Samuel A. Levine of HMS, have identified a new mechanism responsible for the development of fibrosis in the kidney after injury. These findings are published in the May issue of Nature Medicine.
The researchers found a defect in the ability of the surviving cells to divide and replace the damaged cells. This defect is in the cell cycle, and instead of completing cell division, the cells stop their progress through the cell cycle. When stopped at a particular stage, which the investigators identified as the G2/M phase, they produce chemicals which directly and indirectly result in replacement of normal kidney tissue with abnormal fibrotic tissue. When methods were used to enable the cells to move through the cell cycle the fibrosis was prevented.
These results provide new directions for the development of treatments to prevent fibrosis and potentially reduce the number of patients who progress to chronic kidney disease. The development of a new technique to distinguish the various phases of the cell cycle in the kidney after a number of different types of injury proved to be a predictive tool for determining whether kidney injury would result in normal or abnormal repair. If abnormal, fibrosis results and the kidney failure will progress and potentially lead to the need for dialysis.
