Article Text

Download PDFPDF
Vascular impact of progenitor cell mobilisation for cardiac repair post-myocardial infarction
  1. Phillip M Freeman1,
  2. Julian P J Halcox1,2
  1. 1
    University Hospital of Wales, Cardiff, UK
  2. 2
    Wales Heart Research Institute, Cardiff University, UK
  1. Professor Julian Halcox, Wales Heart Research Institute, Cardiff University, Heath Park, Cardiff CF14 4XN, UK; halcoxjp{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Coronary heart disease mortality has been falling steadily over the past four to five decades. In parallel, increasing numbers of people are surviving myocardial infarction (MI) and many face the challenges of a life with heart failure. Indeed, those with substantial myocardial injury often remain symptomatically limited even with aggressive modern management including revascularisation, an optimal medication regimen and, where appropriate, resynchronisation therapy. Immediate reperfusion remains the best way to minimise left ventricular (LV) injury and subsequent dysfunction. However, despite streamlined systems of care and high profile public awareness campaigns all too many myocardial infarctions (MIs) present late or the diagnosis is missed. Thus, development and refinement of novel methodology for the repair of damaged cardiac tissue remain a major priority.

One such strategy is to attempt to harness the body’s own endogenous cellular repair mechanisms. Cell populations with the potential to differentiate into mature cardiovascular cells under appropriate conditions have been identified in the bone marrow and peripheral blood of adult humans. These cells appear to participate in the maintenance of healthy cardiovascular function, although their ability to differentiate into mature cardiac myocytes that integrate into a functional myocardial syncytium remains a controversial and hotly debated issue.1 The biology of these cardiovascular progenitor cells is complex and tightly regulated and there is considerable heterogeneity between individuals in the number and quality of these cells, even for those with similar clinical conditions. These issues pose great challenges to researchers.

Promising early studies in animal models and patients with MI suggest that cell therapy may attenuate LV damage and improve functional capacity, although the benefits appear modest and the exact mechanisms remain unclear at this stage.26 Several cell types have been studied, including unselected or specific fractions of bone marrow-derived or peripheral blood mononuclear cells (PBMCs), which …

View Full Text


  • Competing interests: None.

Linked Articles