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Article

SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis

Retraction in: /10.3892/etm.2024.12779
  • Authors:
    • Jian‑Xia Shi
    • Qi‑Jin Wang
    • Hui Li
    • Qin Huang
  • View Affiliations / Copyright

    Affiliations: Department of Endocrinology, Changhai Hospital, The Second Military Medical University, Shanghai 200433, P.R. China
  • Pages: 342-348
    |
    Published online on: November 30, 2016
       https://doi.org/10.3892/etm.2016.3938
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Abstract

Diabetic nephropathy is a diabetic complication associated with capillary damage and increased mortality. Sirtuin 4 (SIRT4) plays an important role in mitochondrial function and the pathogenesis of metabolic diseases, including aging kidneys. The aim of the present study was to investigate the association between SIRT4 and diabetic nephropathy in a glucose-induced mouse podocyte model. A CCK‑8 assay showed that glucose simulation significantly inhibited podocyte proliferation in a time- and concentration‑dependent manner. Reverse transcription-quantitative polymerase chain reaction and western blot analysis showed that the mRNA and protein levels of SIRT4 were notably decreased in a concentration-dependent manner in glucose‑simulated podocytes. However, SIRT4 overexpression increased proliferation and suppressed apoptosis, which was accompanied by increases in mitochondrial membrane potential and reduced production of reactive oxygen species (ROS). Notably, SIRT4 overexpression downregulated the expression of apoptosis‑related proteins NOX1, Bax and phosphorylated p38 and upregulated the expression of Bcl‑2 in glucose‑simulated podocytes. In addition, SIRT4 overexpression significantly attenuated the inflammatory response, indicated by reductions in the levels of TNF-α, IL-1β and IL‑6. These results demonstrate for the first time that the overexpression of SIRT4 prevents glucose‑induced podocyte apoptosis and ROS production and suggest that podocyte apoptosis represents an early pathological mechanism leading to diabetic nephropathy.
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Copy and paste a formatted citation
Spandidos Publications style
Shi JX, Wang QJ, Li H and Huang Q: SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779. Exp Ther Med 13: 342-348, 2017.
APA
Shi, J., Wang, Q., Li, H., & Huang, Q. (2017). SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779. Experimental and Therapeutic Medicine, 13, 342-348. https://doi.org/10.3892/etm.2016.3938
MLA
Shi, J., Wang, Q., Li, H., Huang, Q."SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779". Experimental and Therapeutic Medicine 13.1 (2017): 342-348.
Chicago
Shi, J., Wang, Q., Li, H., Huang, Q."SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779". Experimental and Therapeutic Medicine 13, no. 1 (2017): 342-348. https://doi.org/10.3892/etm.2016.3938
Copy and paste a formatted citation
x
Spandidos Publications style
Shi JX, Wang QJ, Li H and Huang Q: SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779. Exp Ther Med 13: 342-348, 2017.
APA
Shi, J., Wang, Q., Li, H., & Huang, Q. (2017). SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779. Experimental and Therapeutic Medicine, 13, 342-348. https://doi.org/10.3892/etm.2016.3938
MLA
Shi, J., Wang, Q., Li, H., Huang, Q."SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779". Experimental and Therapeutic Medicine 13.1 (2017): 342-348.
Chicago
Shi, J., Wang, Q., Li, H., Huang, Q."SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis Retraction in /10.3892/etm.2024.12779". Experimental and Therapeutic Medicine 13, no. 1 (2017): 342-348. https://doi.org/10.3892/etm.2016.3938
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