Dr. Yanagita is a Professor in the Department of Nephrology at Kyoto University. Dr. Yanagita’s research efforts are consistently focused on elucidating the mechanisms of kidney disease progression and establishing therapeutic approaches to prevent the progressive loss of kidney function.
Her early work focused on mechanisms of glomerular mesangial cell proliferation, a common finding of glomerular disorders. She identified a product of growth arrest–specific gene 6 (Gas6) as a mesangial cell mitogen and demonstrated that inhibition of Gas6 signaling halts the progression of glomerulonephritis.
Progressive glomerular injury is eventually accompanied by tubulointerstitial damage, whose severity predicts renal prognosis. She demonstrated that the product of uterine sensitization–associated gene 1 (USAG-1) inhibits the renoprotective action of BMP7 and accelerates tubulointerstitial damage as well as glomerular damage. Inhibition of USAG-1 is a promising approach for the development of novel therapies, and the kidney-specific expression of USAG-1 is expected to minimize the risk of adverse effect of USAG-1 inhibition in other tissues.
Renal fibrosis and renal anemia are the common complications in end-stage renal disease. Dr. Yanagita employed a genetic lineage tracing method to demonstrate that erythropoietin-producing cells in healthy kidney and scar-producing myofibroblasts during fibrosis originate from neural crest during embryogenesis. She also demonstrated that the dysfunction of the neural crest–derived fibroblasts is the cause of renal anemia and renal fibrosis and that these two conditions could be reversed by a selective estrogen receptor modulator. These findings highlight a potential therapeutic approach for anemia associated with chronic kidney disease.