Sickle particulars of microparticles

Abstract

Sickle cell disease, caused by a simple single nucleotide mutation, continues to display humbling complexity in its downstream pathophysiology of intravascular hemolysis and inflammatory endothelial response. Polymerization of sickle hemoglobin promotes oxidative stress in red blood cells, with wideranging damage to the red blood cell plasma membrane, cytoskeleton, membrane channels, cytoplasmic metabolites, and antioxidant self-repair mechanisms. Among the subpopulations of red blood cells in sickle cell disease, some expose phosphatidylserine (PS), marking senescent red blood cells for deletion by reticuloendothelial macrophages; this adaptive pathway is called extravascular hemolysis.