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Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
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Pathological Left Ventricular Hypertrophy and Stem Cells: Current Evidence and New Perspectives

Maria E Marketou1, Fragiskos Parthenakis1, Panos E Vardas1

  • 1Cardiology Department, Heraklion University Hospital, P.O. Box 1352, 711 10 Crete, Greece.

Stem Cells International
|January 23, 2016
PubMed

Insights

Stem and progenitor cells are activated in left ventricular hypertrophy (LVH) and contribute to myocardial repair. Their properties suggest potential for regenerative cell therapy in preventing adverse cardiac remodeling.

Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Cardiac Pathophysiology

Background:

  • Left ventricular hypertrophy (LVH) predicts adverse cardiovascular outcomes.
  • LVH involves increased protein synthesis, cell size, and progenitor cell activity.
  • Stem and progenitor cells aid cardiomyocyte renewal after cardiac injury or overload.

Purpose of the Study:

  • To explore the role of stem and progenitor cells in LVH.
  • To investigate their contribution to myocardial repair and remodeling.
  • To assess their potential for regenerative cell therapy.

Main Methods:

  • Review of existing literature on stem/progenitor cells in cardiac hypertrophy.
  • Analysis of cellular mechanisms involved in LVH.
  • Exploration of cell mobilization and differentiation pathways.

Main Results:

  • Stem and progenitor cells are activated in LVH, contributing to cardiomyocyte renewal.
  • These cells secrete factors crucial for cardiac remodeling and neovascularization.
  • Epicardial progenitor cells migrate to the myocardium, participating in cardiac structure formation.
  • Cell mobilization is triggered by mechanical, chemical, hormonal, or pharmacological stimuli.

Conclusions:

  • Stem and progenitor cells play a significant regulatory role in myocardial repair during LVH.
  • Their regenerative potential offers promise for therapeutic interventions against adverse cardiac remodeling.
  • Further research is needed to fully elucidate the underlying pathophysiological mechanisms.

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