Abstract - 2016 Volume.7 Issue.3

We present in this study a theoretical review of Sickle Cell Disease (SCD), highlighting on the pathophysiology and targeted pathways of antisickling products. Sickle cell disease (SCD) is one of the most common genetic disorders worldwide. It is caused by a point mutation that changes glutamic acid (Glu6) to valine (Val6) in the β chain of hemoglobin. This change has many damages: polymerization of abnormal haemoglobin HbS when oxygen tension decreases; red blood cell membrane deformability and cell-to-cell adherence, adhesion of sickle red blood cells to the endothelium, high production of reactive oxygen species (ROS), decreasing lactate dehydrogenase activity and Fe2+/Fe3+ ratio of HbS. Understanding polymerization and pathophysiological of SCD constitute a therapeutic strategy base in the pharmacology research of this molecular disease.

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