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[Vascular endothelial cell dysfunction in diabetes mellitus].

H Fujita1

  • 1Department of Internal Medicine, Tokyo Metropolitan Bokuto General Hospital.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|April 13, 1999
PubMed
Summary
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Advanced Glycation End products (AGE) are key drivers of diabetic vascular complications, including atherosclerosis and retinopathy. Suppressing AGE may offer a novel therapeutic strategy for diabetic angiopathy.

Area of Science:

  • Endocrinology
  • Vascular Biology
  • Ophthalmology

Context:

  • Diabetes mellitus frequently leads to vascular complications like atherosclerosis (macroangiopathy) and retinopathy (microangiopathy).
  • Advanced Glycation End products (AGE) are implicated in atherogenesis via NF-kappa B activation, upregulating VCAM-1 and MCP-1.
  • Diabetic retinopathy involves microangiopathy characterized by angiogenesis, with Vascular Endothelial Growth Factor (VEGF) playing a crucial role.

Purpose:

  • To highlight the significant role of Advanced Glycation End products (AGE) in diabetic vascular disorders.
  • To explore the mechanisms by which AGE contributes to both macroangiopathy and microangiopathy.
  • To propose AGE suppression as a potential therapeutic target for diabetic angiopathy.

Summary:

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  • AGE significantly contributes to atherosclerosis by activating NF-kappa B, leading to increased VCAM-1 and MCP-1.
  • In diabetic retinopathy, AGE, adenosine, and bFGF stimulate retinal cells to produce VEGF.
  • VEGF promotes angiogenesis and vascular permeability in the retina, causing edema and contributing to diabetic retinopathy.

    • Impact:

    • Understanding AGE's role provides insights into diabetic vascular pathology.
    • Identifying AGE as a central factor suggests new therapeutic avenues for managing diabetic complications.
    • Targeting AGE may offer a novel treatment strategy to prevent or mitigate diabetic angiopathy and retinopathy.