Stressed Erythrophagocytosis and its effect in organ injury in Sickle cell disease. Sickled RBCs undergoes untimely senescence and need to be cleared from the circulation by reticuloendothelial macrophages to prevent persistent organ damage. However, it's unclear how senescent RBCs are eliminated. Current research suggests that under stressed conditions the liver is the primary site of RBC clearance. Recent reports have suggested that liver sinusoidal endothelial cells (LSECs) aid in the tethering of aged RBCs within hepatic sinusoids, thus facilitating their engulfment by liver macrophages called kupffer cells (KCs) . Recently, we have shown that SCD mice manifest exacerbated liver senescence and progressive liver injury under baseline conditions. Here, we will use state of the art imaging, molecular biology , biochemistry and advanced omics approaches to identify the mechanism of RBC clearance in SCD liver and effect of RBC senescence in chronic tissue injury.