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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Atherosclerosis as a disease of failed endogenous repair

Andrey G Zenovich1, Doris A Taylor

  • 1Center for Cardiovascular Repair, University of Minnesota, Minneapolis, MN 55455, USA.

Frontiers in Bioscience : a Journal and Virtual Library
|May 30, 2008
PubMed

Insights

Inflammation drives coronary artery disease (CAD). Stem/progenitor cells attempt vascular repair, but age and risk factors impair them, highlighting sex-based differences in CAD treatment strategies.

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Immunology

Background:

  • Coronary artery disease (CAD) remains a leading cause of mortality worldwide.
  • Inflammation is a key pathological mechanism in CAD progression, from endothelial dysfunction to heart failure.
  • Atherosclerosis is increasingly recognized as a disease involving impaired endogenous vascular repair processes.

Purpose of the Study:

  • To explore the role of stem/progenitor cells in vascular repair within the context of CAD.
  • To investigate how aging and cardiovascular risk factors affect progenitor cell function.
  • To examine sex-based differences in progenitor cell capacity and their implications for CAD pathogenesis and treatment.

Main Methods:

  • Review of recent advances in stem/progenitor cell biology and their application in CAD.
  • Identification of key progenitor cell populations involved in vascular repair (e.g., endothelial progenitor cells [AC133+/CD34+], vascular progenitors [CD31+/CD45(low)], KDR+ cells).
  • Analysis of factors influencing progenitor cell efficacy, including age, risk factors, and sex.

Main Results:

  • Stem/progenitor cells are mobilized for vascular repair in CAD.
  • Age and cardiovascular risk factors significantly impair progenitor cell function, even before clinical CAD diagnosis.
  • Emerging evidence suggests sex-based differences in progenitor cell repair capacity may explain clinical CAD disparities between men and women.

Conclusions:

  • Enhancing endogenous vascular repair mechanisms by stem/progenitor cells offers a potential therapeutic avenue for CAD.
  • Understanding the impact of age, risk factors, and sex on progenitor cells is crucial for developing effective, personalized CAD treatments.
  • Quantifying cellular injury and repair processes is key to shifting the balance towards repair and preventing CAD progression.

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