title: Mechanisms and pathophysiological significance of eryptosis, the suicidal erythrocyte death.
abstract: Eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and cell membrane scrambling, is stimulated by Ca(2+) entry through Ca(2+)-permeable, PGE2-activated cation channels, by ceramide, caspases, calpain, complement, hyperosmotic shock, energy depletion, oxidative stress, and deranged activity of several kinases (e.g. AMPK, GK, PAK2, CK1α, JAK3, PKC, p38-MAPK). Eryptosis is triggered by intoxication, malignancy, hepatic failure, diabetes, chronic renal insufficiency, hemolytic uremic syndrome, dehydration, phosphate depletion, fever, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anemia, thalassemia, glucose 6-phosphate dehydrogenase deficiency, and Wilson's disease. Eryptosis may precede and protect against hemolysis but by the same token result in anemia and deranged microcirculation.
authors: Department of Physiology, University of Tübingen, Gmelinstr. 5, 72076 Tübingen, Germany.
authors: Elisabeth
authors: E
authors: Lang
authors: Department of Physiology, University of Tübingen, Gmelinstr. 5, 72076 Tübingen, Germany. Electronic address: florian.lang@uni-tuebingen.de.
authors: Florian
authors: F
authors: Lang
mesh_terms: D000818:Animals; D016923:Cell Death; D002462:Cell Membrane / Q000473:pathology; D016922:Cellular Senescence; D004912:Erythrocytes / Q000473:pathology*; D006801:Humans; D018384:Oxidative Stress
keywords: Chronic kidney disease; Diabetes; Eryptosis; Malaria; Sickle cell disease