Author: Leo
Keywords: chronic kidney disease | chronic kidney disease | marker protein |
key gene | gene knockout
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| From google images |
A recent research group led by John C. He, of the Ian Khan School of Medicine in New York, New York, wrote in Nature Communications that they found that a key protein level would affect kidney health. Further experiments showed that overexpression of RTN1 protein in cultured kidney cells could lead to significant stress and apoptosis in the endoplasmic reticulum.
In the near future, a team led by John C. He, of the Ian Khan School of Medicine in New York, New York, wrote in Nature Communications that they found that a key protein level would affect kidney health. This group found a biomarker protein RTN1 that could promote chronic kidney disease (CKD) more severe. In response to this protein, the researchers believe that the future can regulate the expression of this protein, affecting the development of kidney disease.
Chronic kidney disease (CKD) is common in the adult population of the United States, and it is estimated that 10% of American adults suffer from chronic kidney disease and that the prevalence of this disease has been increasing worldwide. There is no good treatment for chronic kidney disease, and at best there are only a few ways to provide very limited protection that can delay the severity of the disease. This chronic kidney disease eventually causes the patient to have to rely on dialysis, or to undergo kidney transplantation. In mice and humans with chronic kidney disease, the researchers first detected a high expression of RTN1A, a variant of the RTN1 protein. However, on the contrary, in the diabetic nephropathy (diabetic nephropathy) mice and the body, the expression of this protein is very low. This suggests that the expression level of RTN1 protein may be associated with kidney disease.
Further experiments showed that overexpression of RTN1 protein in cultured kidney cells could lead to significant stress and apoptosis in the endoplasmic reticulum. At the same time, by knockout to reduce the expression of RTN1, can lead to tiamycin-induced, hyperglycemia-induced endoplasmic reticulum stress reduction and reduction of apoptosis. RTN1A can interact with PERK with its own N-terminal, C-terminal domain, which can lead to increased stress in the endoplasmic reticulum. For the mutations of RTN1A and PERK protein binding sites, the stress stress of the endoplasmic reticulum was found to be reduced. In mice, the results showed that the knockdown of RTN1A gene in mice, kidney cell endoplasmic reticulum stress reduction, unilateral ureteral obstruction in mice kidney cell fibrosis trend also decreased, at the same time, in small diabetes In vivo, endoplasmic reticulum stress stress is also reduced, proteinuria, glomerular hypertrophy, mesangial expansion and other symptoms have eased.
For the first time, this study has identified a marker protein, RTN1, associated with chronic kidney disease. Overdose expression of a variant of this protein in humans is positively associated with the severity of chronic kidney disease. The mechanism that affects kidney cell health may be that Proteins can cause endoplasmic reticulum stress and increased cell apoptosis. In the future, if we can develop an inhibitor for this protein, reduce the expression of this protein or reduce its physiological activity, perhaps scientific research for chronic kidney disease prevention and treatment to bring new ways.
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