Eryptosis

Eryptosis is the programmed, suicidal death of mature erythrocytes (red blood cells), sharing features with apoptosis in nucleated cells such as cell shrinkage, membrane blebbing, and the loss of membrane phospholipid asymmetry [1, 5]. Because mature erythrocytes lack a nucleus and mitochondria, eryptosis is primarily driven by the activation of non-selective, calcium-permeable cation channels in the cell membrane [2, 8]. The resulting increase in cytosolic calcium (Ca2+) activates scramblases that expose phosphatidylserine (PS) on the outer leaflet and opens Ca2+-sensitive K+ (Gardos) channels, leading to KCl efflux, water loss, and cellular dehydration [3, 7, 8]. While physiological eryptosis serves to eliminate senescent or damaged cells from circulation to prevent hemolysis, excessive eryptosis is triggered by various stressors (e.g., oxidative stress, hyperosmolarity) and numerous drugs [4, 6]. Pathological eryptosis is a key contributor to the development of anemia in conditions like chronic kidney disease, malaria, and diabetes, and it can also impair microcirculation through the adhesion of PS-exposing cells to the vascular wall [4, 9, 12].

Other names

Suicidal erythrocyte deathErythrocyte programmed cell deathErythroptosisEryptosis inducer

Activation of calcium-permeable non-selective cation channels (e.g., TRPC6) leading to calcium influx, which subsequently stimulates phospholipid scramblase (PS exposure) and Gardos channels (KCa3.1) causing cell shrinkage [1, 7, 8].