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Related Experiment Videos

Elastin-elastase-atherosclerosis revisited

L Robert1, A M Robert, B Jacotot

  • 1Université Paris 6, Centre de Recherche Bioclinique sur le Vieillissement, Groupe Hospitalier Charles Foix-Jean Rostand, Ivry sur Seine, France. 106517.545@compuserve.com

Atherosclerosis
|December 23, 1998
PubMed
Summary
This summary is machine-generated.

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Aging alters the vascular extracellular matrix (ECM), promoting atherosclerosis. This review examines age-related ECM changes, lipid interactions, and their impact on vascular function and disease risk.

Area of Science:

  • Cardiovascular Biology
  • Biochemistry
  • Aging Research

Background:

  • The vascular extracellular matrix (ECM) undergoes age-dependent modifications.
  • Atherogenesis is influenced by risk factors like blood lipids and lipoproteins.
  • Previous research has explored these age-related vascular changes.

Purpose of the Study:

  • To review and reinvestigate age-dependent modifications of the vascular ECM.
  • To analyze the relationship between lipids, lipoproteins, and ECM changes in atherogenesis.
  • To integrate decades of laboratory findings with recent publications.

Main Methods:

  • Review of laboratory studies on vascular ECM and atherogenesis.
  • Analysis of age-dependent modifications: elastolytic enzymes, matrix biosynthesis, receptor function.

Related Experiment Videos

  • Confrontation of previous results with recent epidemiological (EVA study) and experimental data.
  • Investigation of lipid-elastin interactions in vitro and in vivo.
  • Examination of elastin laminin receptor function and T-lymphocyte involvement.

    • Main Results:

    • Vascular wall aging involves upregulated elastolytic enzymes and modified matrix biosynthesis.
    • Lipid deposition and lipoproteins alter matrix biosynthesis and upregulate elastase expression.
    • Lipid-elastin interactions show specificity in accumulation.
    • Epidemiological data link blood lipids to matrix components.
    • Elastin laminin receptor function (vasodilation, cholesterol synthesis) declines with age, while elastase release increases.
    • Findings extended to T-lymphocytes in atherosclerotic plaques.

    Conclusions:

    • Aging significantly impacts vascular ECM composition and function, contributing to atherogenesis.
    • Lipid accumulation and altered ECM metabolism are key drivers of age-related vascular disease.
    • Specific molecular mechanisms underlying these age-related vascular changes are elucidated.
    • Understanding these processes offers insights into preventing and treating atherosclerosis.