Abstract(s)
Aging is associated with an increased incidence of cardiovascular disease and
thrombosis. Platelets play a major role in maintaining hemostasis and in thrombus
formation, making them a key player in thrombotic disorders. Whereas it is well-known
that platelet aggregability is increased in vascular diseases, the contribution of
age-related changes in platelet biology to cardiovascular risk is not well-understood.
Several lines of evidence support that platelets from older subjects differ in their function
and structure, making platelets more prone to activation and less sensitive to inhibition.
These age-related changes could lead to platelet hyperactivity and to the development
of a prothrombotic state in advanced age. This review will focus on platelet biochemical
modifications during aging and on the mechanisms by which these alterations could lead
to thrombotic disease.