CarDiovascular Disease

  • Condition

Cardiovascular disease (CVD) is a major public health concern that is responsible for approximately 17.5 million deaths per year of which 80% of these are due to myocardial infarctions and strokes (WHO). This factor has led to more research on stem cell therapies for regenerative solutions that provide much more than what is currently offered by conventional drugs or medicine. By addressing the problem at an early stage, it might be possible to reduce the secondary deterioration seen in patients after an acute injury, or even a slowly progressive degeneration might be preventable in the future. With time there is a reduction in the repairing effects of endogenous cells mainly caused by age (Rauscher et al 2003), comorbidities (Higashi et al 2012) and genetics.

CDV has to be addressed by areas such as cardiac muscle and endothelial and smooth muscle cells. There are different cells that must be included to achieve a complete regenerative result in regards with CVD. There endothelial progenitor cells that are responsible for vascular repair and angiogenesis (Shantsila et al 2007). We now know that the aging process in all humans has a direct effect on bone marrow cells, reducing the number (Hill et al 2003), presenting dormant cells even upon injury and reduction in migration of cells to injured sites and affecting the differentiation of these cells to committed lines which may contribute to atherosclerosis and cardiovascular disease. It is obvious to target this deficiency and research is being held in clinical settings (Goto et al 2016).

The myocardium was believed to have a predetermined number of cardiomyocytes after birth without presenting the ability to repair. However, it was found that throughout life we preserve a pool of Cardiac progenitor cells (CPCs)(Anversa et al 2002; Beltrami et al 2003). And therefore, after acute injury, there is differentiation and regeneration by endogenous cells reducing the extension of the injury (Rooji, 2016; Urbanek et al 2005).

Mesenchymal stem cells are multipotent cells capable of differentiating into several cell lines. They are derived mainly from the stroma of bone marrow, however, there are other sources. In clinical studies, Myocardial Infarction patients improve with administration of MSCs (Hare et al 2009; Trivedi et al 2010). Their first intended use was to graft to damaged tissue and differentiate. However, the improvement seen was more attributable to a paracrine effect and increase in angiogenesis (Boyle et al 2006).

The material that you just read comes from the following links.


  • Anversa P, Nadal-Girard B. Myocyte renewal and ventricular remodeling. Nature 2002;415:240-243.
  • Beltrami AP,  et al. Adult cardiac stem cells are multipotent and support myocardial regeneration. Cell 2003;114:763-776.
  • Boyle AJ, Schulman SP, Hare JM, Controversies in Cardiovascular Medicine: Stem Cell Therapy for Cardiac Repair. Circulation 2006:114:339-352.
  • Burridge PW, Zambidis ET, Highly efficient directed differentiation of human induced pluripotent stem cells into cardiomyocytes. Methods MolBiol 2013;997:149-161.
  • Hare JM, Traverse JH, et al. A randomized, double-blind, placebo controlled, dose-escalation study of intravenous adult human mesenchymal stem cells (prochymal) after acute myocardial infarction. J Am CollCardiol 2009; 54(24):2277-2286.
  • Rauscher FM, Golsdchmidt-Clermont PJ, et al. Aging, Progenitor Cell Exhaustion, and Atherosclerosis. Circulation 2003;108:457-463.
  • Rooji E. Cardiac Repair after Myocardial Infarction. N Engl J Med 2016;374:85-87.
  • Shantsila E,, Watson T, Lip GYH, Endothelial Progenitor Cells in Cardiovascular Disorders. Journal of the American College of Cardiology, 2007; 49(7):741-752.
  • Trivedi P, Tray N, et al. Mesenchymal stem cell therapy for treatment of Cardiovascular disease: helping people sooner or later. Stem cells Dev 2010;19(7):1109-1120.
  • Urbanek K, TorellaD, et al. Myocardial regeneration by activation of multipotent cardiac stem cells in ischemic heart failure. Proc Natl Acad Sci U S A  2005;102:8692-8697.
  • World Health Organization. Revised on June 2016.

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