Similar to apoptosis of nucleated cells, suicidal erythrocyte death or eryptosis is characterized by cell shrinkage, membrane blebbing and membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Signaling of eryptosis involves formation of prostaglandin E-2 with subsequent activation of cation channels and Ca2+-entry and/or release of platelet activating factor (PAF) with subsequent activation of sphingomyelinase and formation of ceramide. Ca2+ and ceramide stimulate cell membrane scrambling. Ca2+ further activates Ca2+ sensitive K+-channels leading to cellular KCl loss and cell shrinkage and stimulates the protease calpain resulting in degradation of the cytoskeleton. Injuries triggering eryptosis may similarly compromise survival of nucleated cells. The case is made that analysis of enhanced eryptosis may direct to the pathophysiology of systemic disease. Examples presented include drug side effects, sepsis, haemolytic uremic syndrome, Wilson's disease, phosphate depletion and a rare condition caused by a mutation in GLUT1 turning the carrier into a cation channel.
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机译：类似于有核细胞的凋亡，自杀性红细胞死亡或加密的特征是细胞收缩，膜起泡和膜磷脂在细胞表面暴露于磷脂酰丝氨酸。加密的信号传导涉及前列腺素E-2的形成和随后阳离子通道的激活，以及Ca2 +的进入和/或血小板激活因子（PAF）的释放以及鞘磷脂酶的激活和神经酰胺的形成。 Ca2 +和神经酰胺刺激细胞膜的争夺。 Ca 2+进一步激活Ca 2+敏感的K +通道，导致细胞KCl丢失和细胞收缩，并刺激蛋白酶钙蛋白酶，导致细胞骨架降解。触发加密的损伤可能同样损害有核细胞的存活。事实证明增强加密的分析可能直接作用于全身性疾病的病理生理。所列举的例子包括药物副作用，败血症，溶血性尿毒症综合征，威尔逊氏病，磷酸盐耗竭以及由GLUT1突变导致载体变成阳离子通道的罕见情况。
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