High glucose inhibits renal proximal tubule cell proliferation and involves PKC, oxidative stress, and TGF-beta 1

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Updated: Oct 8, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

S H Park1, H J Choi, J H Lee

  • 1Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Kwangju, Korea.

Kidney International
|April 25, 2001
PubMed
Abstract

Insights

High glucose inhibits renal proximal tubule cell proliferation through protein kinase C (PKC) and oxidative stress, involving transforming growth factor-beta1 (TGF-beta1) signaling. This mechanism is crucial for understanding diabetic nephropathy progression.

Area of Science:

  • Nephrology
  • Cell Biology
  • Endocrinology

Background:

  • Diabetic nephropathy is characterized by altered renal cell growth.
  • The precise mechanisms of high glucose effects on renal proximal tubule cell (PTC) proliferation remain unclear.

Purpose of the Study:

  • To investigate the impact of high glucose on PTC proliferation.
  • To elucidate the underlying molecular mechanisms, including protein kinase C (PKC) and oxidative stress pathways.

Main Methods:

  • Primary cultured renal PTCs were exposed to 25 mmol/L glucose.
  • Assessed cell proliferation, DNA/protein synthesis, cell cycle, and lipid peroxide formation.
  • Investigated the role of antioxidants, PKC inhibitors, and transforming growth factor-beta1 (TGF-beta1).

Main Results:

  • High glucose (25 mmol/L) inhibited thymidine incorporation and cell growth but increased leucine incorporation and protein content.
  • Elevated lipid peroxide formation was observed, which was ameliorated by antioxidants and PKC inhibitors.
  • High glucose stimulated PKC translocation and TGF-beta1 secretion, with TGF-beta1 inhibiting cell proliferation.

Conclusions:

  • High glucose inhibits renal PTC proliferation via a pathway involving PKC, oxidative stress, and TGF-beta1.
  • These findings provide insights into the cellular mechanisms of diabetic nephropathy.

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