Friday, June 8, 2012

Drug target for treatment of nephrotic


The scientists found a kidney disease can lead to kidney failure and other reasons, this finding may be able to bring a drug target for the treatment of chronic kidney disease.Focal segmental glomerulosclerosis (referred to as FSGS) is characterized by lesions and hardening of the tiny blood vessels in the kidneys, resulting in protein penetrate into the urine. There are no effective method for the treatment of FSGS, and its incidence is also increasing. By studying a large family of hereditary FSGS, Michelle Winn, and colleagues in the coding of a found a mutation in the gene of calcium into the cell protein.This ion channel proteins called transient receptor potential cation channel 6 or TRPC6.Because ion channels are usually susceptible to the influence of drugs, so this work will TRPC6 as a drug target for the treatment of chronic kidney disease a possibility.Previous studies have revealed that interrupt cytoskeletal and structural proteins of FSGS development process works.
Duke University Medical Center researchers have discovered a gene related to the type of chronic kidney disease. This disease called FSGS (familial focal segmental glomerulosclerosis) can cause complete renal failure, and affects 20% of dialysis patients. This finding will promote more effective treatment of this disease.
By the genetic composition of the detection of more than one multigenerational family with important types of FSGS, the researchers found something called TRPC6 (Transient Cycle Receptor Potential Cation Channel 6), a mutant form of the gene associated with the disease. Moreover, the function of this gene and related genes previously found in FSGS, these findings reveal a novel mechanism of renal injury. Targeting this ion channel drugs may effectively alleviate or prevent the scarring of the kidney. These channels are embedded in the membrane pore-like protein, able to control calcium flow. This gene represents the first with FSGS related ion channels. Winn et al. These findings are published in the May 5 online edition of Science magazine.
In the United States of FSGS incidence rate increases every year, and drug treatment of this disease is very limited and are non-specific drugs. So many patients to rely on dialysis to prolong life. Of FSGS etiology remains unclear, but previous findings suggest that the three other genes related with FSGS or class of FSGS disease. Previously identified genes responsible for the formation of the support membrane structural proteins. In 1999, the Duke research group identified in a New Zealand family with FSGS-related genomic regions.
In the latest study, researchers screened 106 individuals in seven generations and 600 members of the family, this narrowed it down to an exact gene - TRPC6. In this family, all FSGS members carry a TRPC6 gene mutation. Further study of variants of this gene in cultured kidney cells, this mutation responsible for the regulation of angiotensin II channel activity, angiotensin II can promote the occurrence of hypertension and kidney damage.
Although there are reports that TRPC6 mutations found in other hereditary FSGS family, but the findings on the role of this channel in kidney function problems bubbling to the surface. This channel may also be a new target for treatment of kidney disease.

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