Hyperglycemia alters renal cell responsiveness to pressure in a model of malignant hypertension

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

Published on: May 2, 2025

Shai Efrati1, Sylvia Berman, Yariv Siman Tov

  • 1Research and Development Department, Assaf Harofeh Medical Center, Zerifin, Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Israel.

Journal of Hypertension
|January 22, 2009
PubMed
Abstract

Insights

High glucose and malignant hypertension worsen kidney injury through different pathways. Hyperglycemia increases apoptosis via p53, while hypertension uses angiotensin-II, impacting cell proliferation and injury.

Area of Science:

  • Nephrology
  • Endocrinology
  • Cell Biology

Background:

  • Diabetic nephropathy is a major complication of poor glycemic control.
  • Mechanisms of high glucose-induced renal injury are not fully understood.
  • Malignant hypertension exacerbates renal tissue damage.

Purpose of the Study:

  • Investigate renal cell subset responses to hyperglycemia and pressure.
  • Elucidate mechanisms of high glucose-aggravated renal injury in vitro.
  • Model malignant hypertension effects on hyperglycemic renal cells.

Main Methods:

  • Rat renal mesangium, epithelium, and endothelium cultured in high glucose medium.
  • Cells subjected to high hydrostatic pressure simulating malignant hypertension.
  • Assessed proliferation, apoptosis, p53, H2O2, and angiotensin-II synthesis.

Main Results:

  • Hyperglycemic cells showed increased p53, angiotensin-II, and apoptosis, with depressed proliferation.
  • High pressure increased H2O2 release, further elevated by high glucose.
  • Inhibition of p53 reduced apoptosis in hyperglycemic cells.

Conclusions:

  • Hyperglycemia alters renal cell response to simulated malignant hypertension.
  • Both conditions increase apoptosis, but via distinct pathways (p53 vs. angiotensin-II).
  • Hyperglycemia inhibits pressure-induced proliferation and maximally augments angiotensin-II production.

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