Researchers from Mount Sinai School of Medicine have identified a regulator protein that plays a crucial role in kidney fibrosis, a condition that leads to kidney failure, according to a report published this week in Nature Medicine. Finding this regulator provides a new therapeutic target for millions of Americans affected by kidney failure. The research team studied three mouse models of kidney fibrosis: one group of mice contained HIV viral proteins incorporated into their genome; the second group was injected with a high dose of folic acid; in the third mouse model, kidney filtration was blocked in one kidney. All of these factors cause kidney fibrosis. The researchers gathered the genetic material of the mice and compared it to the genetic material of mice that did not have kidney fibrosis. Using a new computational systems biology algorithm and software, the results from these experiments were analyzed. They found that HIPK2, a protein kinase, or regulator, was highly active in the mice with kidney fibrosis. HIPK2 regulates the way certain genes are expressed and when HIPK2 is highly active this leads to kidney fibrosis. The researchers also found that when they eliminated HIPK2, fibrosis was less prominent and the condition of the mice significantly improved. \"Our findings have important implications for people with kidney diseases, patients I treat every day,\" said lead author John Cijiang He. \"Protein kinases like HIPK2 are highly effective therapeutic targets. We look forward to exploring this further.\"