SENDAI, Japan -- Clues to the cause of sometimes fatal crescentic glomerulonephritis, and a possible therapeutic target, may have been uncovered by a mutation in a strain of experimental mice.
SENDAI, Japan, Aug. 31 -- Clues to the cause of sometimes fatal crescentic glomerulonephritis may have been uncovered by a mutation in a strain of experimental mice.
What's more, the mutant mice may have revealed a possible therapeutic target, according to Masao Ono, M.D., of the Tohoku University Graduate School of Medicine here.
The key factor appears to be impaired platelet function, Dr. Ono and colleagues reported in the September issue of Arthritis & Rheumatism, and the potential target of therapy is a protein complex dubbed BLOC-1.
The researchers had been studying an inbred strain of mice that reliably develops crescentic glomerulonephritis in hopes of understanding the pathogenesis of the disease, when a spontaneous mutation developed among the experimental animals.
The mutant animals lived twice as long as their cousins and by the time they were 12 to 16 weeks old they had significantly reduced (at P
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