Cardiac myocytes and fibroblasts exhibit differential sensitivity to apoptosis-inducing stimuli

  • Edward G. Lakatta
  • Xilin Long
  • Alan Chesley
  • Michael Crow
Part of the Basic Science for the Cardiologist book series (BASC, volume 5)


Cell death in the cardiovascular system by apoptosis has received considerable attention in recent years. Cardiac and vascular cell death by apoptosis is not only a feature of embryologic and neonatal development, but can be elicited by a variety of diverse stimuli (Table I) and has been linked to virtually every major cardiovascular disease or disorder (Table II). In many of these disorders, particularly those leading to chronic heart failure, myocyte cell death/loss is usually accompanied by an increase in fibrous tissue content (1). Excessive fibrosis in the presence of myocyte loss has been advocated as a basis for impaired myocardial function in these disease states. The spontaneous hypertensive rat presents a clear example of the imbalance that exists as heart failure evolves (2). In this experimental model, increased cardiac myocyte apoptosis (Figure 1C) can be linked to the reduction in myocyte fractional mass (Figure 1A) as the hearts progress to failure. During this same time, there is a substantial increase in the fibrotic fractional area of the heart (Figure IB).


Proliferate Cell Nuclear Antigen Cardiac Myocytes Cardiac Fibroblast Recombinant Adenovirus Cardiomyocyte Apoptosis 
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Copyright information

© Kluwer Academic Publishers 2000

Authors and Affiliations

  • Edward G. Lakatta
    • 1
  • Xilin Long
    • 1
  • Alan Chesley
    • 1
  • Michael Crow
    • 1
  1. 1.National Institute of HealthBaltimoreUSA

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