Open Access

PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism

  • Authors:
    • Liwen Zhang
    • Jian Liu
    • Fangfang Zhou
    • Weiming Wang
    • Nan Chen
  • View Affiliations

  • Published online on: January 16, 2018     https://doi.org/10.3892/mmr.2018.8433
  • Pages: 4490-4498
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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 γ (PPARγ) coactivator‑1α (PGC‑1α) participates in mitochondrial biogenesis and energy metabolism in certain mitochondria‑enriched cells, including myocardial and skeletal muscle cells. Therefore, we hypothesized that PGC‑1α 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 PPARγ agonist rosiglitazone was employed to induce PGC‑1α 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‑1α 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‑1α expression exhibited protective effects against oxidative stress, glomerulosclerosis and tubulointerstitial fibrosis in experimental DKD. These results indicated a potential role of PGC‑1α in the amelioration of key pathophysiological features of DKD and provided evidence for PGC‑1α as a potential therapeutic target in DKD.
View Figures
View References

Related Articles

Journal Cover

March-2018
Volume 17 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang L, Liu J, Zhou F, Wang W and Chen N: PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism. Mol Med Rep 17: 4490-4498, 2018
APA
Zhang, L., Liu, J., Zhou, F., Wang, W., & Chen, N. (2018). PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism. Molecular Medicine Reports, 17, 4490-4498. https://doi.org/10.3892/mmr.2018.8433
MLA
Zhang, L., Liu, J., Zhou, F., Wang, W., Chen, N."PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism". Molecular Medicine Reports 17.3 (2018): 4490-4498.
Chicago
Zhang, L., Liu, J., Zhou, F., Wang, W., Chen, N."PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism". Molecular Medicine Reports 17, no. 3 (2018): 4490-4498. https://doi.org/10.3892/mmr.2018.8433