In the study, when researchers compared biopsy samples from healthy kidneys and kidneys from people with DNP and FSGS, they found that the Notch pathway was active in diseased but not in healthy kidneys.
Susztak and colleagues bred a strain of mice in which they could specifically activate the Notch pathway within podocytes.
The results showed that the podocytes in these mice underwent programmed cell death, and the mice themselves died from end-stage renal failure.
The researchers also found that after they induced glomerular disease in mice by injecting them with a toxic chemical, they were able to protect the rats from developing kidney disease by injecting them with a gamma secretase inhibitor, one of a class of compounds known to 'shut off' the Notch pathway.
Susztak and colleagues noted that gamma secretase inhibitors, similarly the one that protected the mice from kidney disease, are already in clinical trials for treating diseases including Alzheimer's and leukemia.
According to researchers, the findings "provide some hope that researchers in the field of kidney disease can reverse the grim record of the last 20 years - during which no new therapeutic agent has been successfully implemented" for treating end-stage kidney disease.
The study is published in the March issue of Nature Medicine.
Source-ANI
SRM/L