Erythrocyte senescence and catabolism describe how the roughly 100–120 day lifespan of a red blood cell is terminated by progressive degradation of its membrane cytoskeleton — principally spectrin and ankyrin, with accessory proteins glycophorin, band 3, and proteins 4.1 and 4.2 — causing loss of deformability, entrapment in the sinusoidal capillaries of spleen, liver, and bone marrow, and phagocytosis by macrophages. Macrophage enzymes cleave hemoglobin into globin, which is proteolyzed to recyclable amino acids, and heme, which yields iron for storage as ferritin (apoferritin plus iron) and hemosiderin or export via ferroportin and transferrin, plus a porphyrin remnant converted to biliverdin and then bilirubin. Within hematology and its intersection with hepatobiliary physiology, the resulting bilirubin metabolism — albumin-bound unconjugated transport, hepatic conjugation with glucuronic acid, biliary excretion, bacterial conversion to urobilinogen, enterohepatic recycling, and terminal oxidation to urobilin and stercobilin — establishes the theoretical basis for interpreting pigment distribution in plasma, urine, and feces.
Erythrocyte senescence and catabolism describe how the roughly 100–120 day lifespan of a red blood cell is terminated by progressive degradation of its membrane cytoskeleton — principally spectrin an…