4.4 Article

Overexpression of NDUFV1 alleviates renal damage by improving mitochondrial function in unilateral ureteral obstruction model mice

期刊

CELL BIOLOGY INTERNATIONAL
卷 46, 期 3, 页码 381-390

出版社

WILEY
DOI: 10.1002/cbin.11736

关键词

mitochondria; NDUFV1; nephropathy; oxidative stress; unilateral ureteral obstruction

资金

  1. Natural Science Foundation of China [82170750]
  2. Natural Science Foundation of Jiangsu Province [BK20201210]
  3. Health and Family Planning Commission research projects of Jiangsu [H201522]
  4. Science and Technology Foundation of Nantong [BK2013006]

向作者/读者索取更多资源

NDUFV1 plays a beneficial role in improving kidney function, maintaining renal structures, and alleviating renal fibrosis in UUO model mice. The study suggests that ETC complex I is important for dealing with acute kidney injury and other mitochondrial-associated renal diseases.
Mitochondrial homeostasis plays essential role for the proper functioning of the kidney. NADH-ubiquinone oxidoreductase core subunit V1 (NDUFV1) is an enzyme in the complex I of electron transport chain (ETC) in mitochondria. In the present study, we examined the effects of NDUFV1 on renal function in unilateral ureteral obstruction (UUO) model mice. Our data showed that increased expression of NDUFV1 improves kidney function as evidenced by the decreases in blood urea nitrogen and serum creatinine in UUO mice. Moreover, NDUFV1 also maintains renal structures and alleviates renal fibrosis induced by UUO surgery. Mechanistically, NDUFV1 mitigates the increased oxidative stress in the kidney in UUO model mice. Meanwhile, increased expression of NDUFV1 in the kidney improves the integrity of the complex I and potentiates the complex I activity. Overall, these results indicate that the ETC complex I plays a beneficial role against renal dysfunction induced by acute kidney injury such as UUO. Therefore, NDUFV1 might be a druggable target for developing agents for dealing with disabled mitochondria-associated renal diseases.

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