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Multilevel Microdissection and Functional-Structural Profiling of Human Renal Arterial Branches
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Frontiers in nephrology: early atherosclerosis--a view beyond the lumen

Mario Gossl1, Lilach O Lerman, Amir Lerman

  • 1Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Journal of the American Society of Nephrology : JASN
|October 12, 2007
PubMed

Insights

Microvascular endothelial dysfunction, involving the vasa vasorum and endothelial progenitor cells, may precede macrovascular issues in coronary artery disease. Therapies targeting these micro-aspects offer future cardiovascular disease prevention.

Area of Science:

  • Cardiovascular Medicine
  • Vascular Biology
  • Atherosclerosis Research

Background:

  • Endothelial dysfunction is a key marker for early coronary artery disease (CAD), linked to increased cardiovascular risk.
  • Emerging concepts highlight microvascular and microcellular aspects of endothelial dysfunction preceding macrovascular changes.
  • Proatherosclerotic changes in the vasa vasorum and endothelial progenitor cells (EPCs) may occur before evident CAD.

Purpose of the Study:

  • To introduce and define microvascular endothelial dysfunction and microcellular endothelial dysfunction.
  • To explore the role of vasa vasorum neovascularization and EPCs in early CAD.
  • To propose future therapeutic strategies targeting microvascular and microcellular pathways.

Main Methods:

  • Review of recent research on endothelial dysfunction in CAD.
  • Conceptualization of microvascular and microcellular endothelial dysfunction.
  • Discussion of vasa vasorum function and EPCs' role in atherogenesis.

Main Results:

  • Microvascular endothelial dysfunction (vasa vasorum) and microcellular endothelial dysfunction (EPCs) may precede macrovascular endothelial dysfunction.
  • Vasa vasorum neovascularization contributes to vessel wall inflammation and substance influx.
  • Impaired EPC mobilization and function are implicated in CAD.

Conclusions:

  • Microvascular and microcellular endothelial dysfunction represent early pathogenic mechanisms in CAD.
  • Targeting vasa vasorum and EPCs offers novel therapeutic avenues for CAD prevention.
  • Future interventions should focus on mitigating microvascular and microcellular endothelial dysfunction.

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