Polymerization of deoxy sickle cell hemoglobin (HbS) is well recognized as the primary
event that triggers the classic cycles of sickling/unsickling of patients red blood cells (RBCs).
RBCs are also subjected to continuous endogenous and exogenous oxidative onslaughts
resulting in hemolytic rate increases which contribute to the evolution of vasculopathies
associated with this disease. Compared to steady-state conditions, the occurrences of vaso-
occlusive crises increase the levels of both RBC-derived microparticles as well as …