SIRT2 Affects Cell Proliferation and Apoptosis by Suppressing the Level of Autophagy in Renal Podocytes

Shuang Liu1, Xiangfu Gao2, Zhenliang Fan3

  • 1Geriatrics, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

Disease Markers
|May 2, 2022
PubMed
Abstract

Insights

SIRT2 expression increases in high glucose conditions, impairing kidney cell function. Reducing SIRT2 improves cell proliferation and autophagy, suggesting it as a therapeutic target for diabetic kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Diabetic nephropathy management remains challenging despite molecular discoveries.
  • Limited progress in drug design for diabetic kidney diseases necessitates novel therapeutic targets.

Purpose of the Study:

  • To investigate the expression of SIRT2 in high-glucose murine kidney cells.
  • To determine the impact of SIRT2 on kidney cell biological functions, including proliferation, apoptosis, and autophagy.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to detect SIRT2 expression.
  • CCK8 assay and flow cytometry for cell proliferation and apoptosis analysis.
  • Western blotting for autophagy markers and chloroquine treatment to assess SIRT2's role.

Main Results:

  • SIRT2 expression was significantly upregulated in high-glucose conditions.
  • High glucose reduced cell proliferation and autophagy while increasing apoptosis.
  • Knocking down SIRT2 reversed these effects, enhancing proliferation and autophagy and reducing apoptosis.

Conclusions:

  • SIRT2 is upregulated in hyperglycemic kidney cells and influences cell proliferation and apoptosis.
  • SIRT2 may regulate cell autophagy, presenting a potential therapeutic pathway for diabetic kidney disease.

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