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: Elisabeth Lang, Florian Lang
• Journal: Seminars in cell & developmental biology (Semin Cell Dev Biol) Vol. 39 Pg. 35-42 (Mar 2015) ISSN: 1096-3634 [Electronic] England
• PMID: 25636585 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2015 Elsevier Ltd. All rights reserved.

Topics

• Animals
• Cell Death
• Cell Membrane (pathology)
• Cellular Senescence
• Erythrocytes (pathology)
• Humans
• Oxidative Stress