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FBW7 Regulates the Autophagy Signal in Mesangial Cells Induced by High Glucose

Chenlin Gao1,2, Fang Fan1,3, Jiao Chen4

  • 1Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Sichuan 646000, China.

Biomed Research International
|May 24, 2019
PubMed
Abstract

Insights

FBW7 (F-box and leucine-rich repeat protein 5) downregulation in high glucose conditions impairs autophagy in diabetic nephropathy. Overexpressing FBW7 restores autophagy, reduces inflammation, and mitigates fibrosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Nephrology

Background:

  • Diabetic nephropathy (DN) involves abnormal autophagy regulation.
  • The mechanistic target of rapamycin (mTOR) pathway is a key negative regulator of autophagy.
  • FBW7 (F-box and leucine-rich repeat protein 5) targets mTOR for degradation, influencing autophagy.

Purpose of the Study:

  • To investigate the role of FBW7 in diabetic nephropathy.
  • To explore the relationship between FBW7, autophagy, and mTOR signaling in renal mesangial cells.
  • To examine the therapeutic potential of modulating FBW7 in vitro.

Main Methods:

  • Cultured human renal mesangial cells under high glucose conditions.
  • Utilized FBW7 gene overexpression and rapamycin (mTOR inhibitor).
  • Assessed autophagy markers, inflammatory cytokines, and fibrotic factors via Western blot, ELISA, RT-PCR, and immunofluorescence.

Main Results:

  • High glucose reduced FBW7 expression, activated mTOR, and suppressed autophagy.
  • FBW7 overexpression inhibited mTOR signaling, enhanced autophagy, and decreased inflammatory and fibrotic markers.
  • Rapamycin treatment mimicked some effects of FBW7 overexpression by inhibiting mTOR.

Conclusions:

  • FBW7 expression is decreased in high glucose-induced mesangial cells.
  • FBW7 upregulation enhances autophagy by inhibiting mTOR signaling.
  • FBW7 overexpression demonstrates potential in ameliorating inflammation and fibrosis in diabetic nephropathy.

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