期刊
MOLECULAR MEDICINE REPORTS
卷 17, 期 3, 页码 4490-4498出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2018.8433
关键词
peroxisome proliferator-activated receptor coactivator-1; diabetic kidney disease; oxidative damage
资金
- National Key Research and Development Program of China [2016YFC1305402]
- National Natural Science Foundation of China [81270782, 30771000]
- Research Project of Science and Technology Commission of Shanghai Municipality [15140902800]
- Key Projects of National Basic Research Program of China 973 [2012CB517701]
- National Key Technology RD Program [2011BAI10B00]
The production of reactive oxygen species (ROS) is a common phenomenon in podocyte impairment, which leads to the irreversible progression of chronic kidney diseases, such as diabetic kidney disease (DKD). Previous research has indicated that peroxisome proliferator-activated receptor (PPAR) coactivator-1 (PGC-1) participates in mitochondrial biogenesis and energy metabolism in certain mitochondria-enriched cells, including myocardial and skeletal muscle cells. Therefore, we hypothesized that PGC-1 may be a protective nuclear factor against energy and oxidative stress in DKD. To investigate this hypothesis, db/db diabetic mice were used to establish a DKD model and the PPAR agonist rosiglitazone was employed to induce PGC-1 expression in vivo. Additionally, immortalized mouse podocytes and SV40 MES 13 renal mesangial cells were utilized for in vitro experiments. The expression levels of PGC-1 and genes associated with kidney and cell injury were determined by western blotting or reverse transcription-quantitative polymerase chain reaction and intracellular ROS levels were assessed by 2,7-dichlorodihydrofluorescein diacetate. The results of the present study demonstrated that endogenous PGC-1 expression exhibited protective effects against oxidative stress, glomerulosclerosis and tubulointerstitial fibrosis in experimental DKD. These results indicated a potential role of PGC-1 in the amelioration of key pathophysiological features of DKD and provided evidence for PGC-1 as a potential therapeutic target in DKD.
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