Clonal hematopoiesis and atherosclerosis

European Coordinator:
  • Oliver SOEHNLEIN, Ludwig Maximilians University, München (Germany)
North American Coordinator:
  • Alan TALL, Columbia University Medical Center, New York (USA)
  • Benjamin EBERT, Harvard Medical School, Boston (USA)
  • Siddhartha JAISWAL, Stanford University, Palo Alto (USA)
  • Steffen MASSBERG, Ludwig-Maximilians-University, München (Germany)
  • Andrés HIDALGO, Spanish National Center for Cardiovascular Research, Madrid (Spain)
  • José Javier FUSTER ORTUÑO, Centro Nacional de Investigaciones Cardiovasculares Carlos III (F. S. P), Madrid (Spain)
  • Ira TABAS, Columbia University Medical Center, New York (USA)

The production of blood cells is called hematopoiesis. Hematopoietic stem cells are the precursor, or progenitor, cells in the bone marrow which ultimately give rise to the blood cells that normally circulate in our blood. When a unique mutation occurs in a stem cell’s DNA (the genetic material) a larger than normal number of blood cells will be produced from that single stem cell. It is thought that the resulting subpopulation of blood cells is “clonally” derived from a single founding cell and is therefore made of genetic “clones” of the founder.Clonal hematopoiesis may occur in people who are completely healthy but has also been found in people with hematologic (blood) diseases. The incidence of clonal hematopoiesis has been found to rise dramatically with age. Recent studies have demonstrated that less than 1% of the population under age 40 but approximately 10-20% of the population over age 70 has observable clonal hematopoiesis. Clonal hematopoiesis does not typically give rise to noticeable symptoms, but does lead to increased risk of cardiovascular disease. This Leducq network will investigate genetic and environmental factors that promote the development of clonal hematopoiesis, explore how clonal hematopoiesis increases the development of atherosclerosis and subsequent heart disease, and determine how to modify the impact of the clones on cardiovascular disease in humans.