期刊
NEPHRON EXPERIMENTAL NEPHROLOGY
卷 111, 期 4, 页码 E73-E79出版社
KARGER
DOI: 10.1159/000209207
关键词
Notch; Podocytes; Glomerulosclerosis; Albuminuria; gamma-Secretase inhibitors
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK076077] Funding Source: NIH RePORTER
- NIDDK NIH HHS [R01 DK076077-01A1, R01 DK076077, R01 DK076077-03, R01 DK076077-02] Funding Source: Medline
Podocytes play a key role in the maintenance of the glomerular filtration barrier. Depletion or dysregulative mechanisms of podocytes can lead to the development of glomerulosclerosis. Signaling pathways that control these processes in podocytes are not fully understood. Recent studies from our and other laboratories found that genes that belong to the Notch pathway are regulated in patients and in animal models of renal disease. Genetic studies performed on mice with conditional expression of active Notch1 protein showed massive albuminuria, glomerulosclerosis, and ultimately renal failure and death of the animals. gamma-Secretase inhibitors and genetic deletion of Notch transcriptional binding partner (Rbpj) protected animals from nephrotic syndrome. Further studies are needed to define whether the activation of Notch pathway in podocytes represents a common pathomechanism in glomerular injury, and its potential to be a therapeutic target for the treatment of chronic kidney disease. Copyright (C) 2009 S. Karger AG, Basel
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