摘要
在衰老之前,红细胞可能会经历损伤,包括其损伤完整性从而引发自杀性红细胞凋亡或发生黑色素沉着。这种机制的特征在于细胞收缩、细胞膜气泡和磷脂酰丝氨酸暴露于巨噬细胞鉴定的细胞表面上的细胞膜磷脂,其吞噬并降解了色素细胞。术语密码学还包括典型的机制,其有助于触发这一过程,例如氧化应激、钙离子进入与细胞溶质钙离子活性的增加以及p38激酶的活化,p38激酶是在人红细胞、高渗性休克后活化。已经在几种临床病症如糖尿病、肾功能不全、溶血性尿毒综合征、败血症、支原体感染、弩机、缺铁、镰状细胞性贫血、β-地中海贫血、葡萄糖-6-磷酸脱氢酶(G6PD)遗传性球状红细胞增多症、阵发性夜间血红蛋白尿、威尔逊病、骨髓增生异常综合征和磷酸盐消耗。因此,可以人为色素破坏是去除有缺陷的红细胞以防止溶血的有用机制。此外,感染的红细胞在诸如疟疾等疾病中可能会抵消寄生虫血症。事实上,已知镰状细胞形状,β-地中海贫血、葡萄糖-6-磷酸脱氢酶和铁缺乏可以对严重的疟疾进行一定的保护。重要的是,通过诱导色素沉淀来控制疟原虫感染的策略预计不会产生病原体的抗性,因为参与宿主细胞自杀性死亡的蛋白质不是由病原体编码的,因此不能通过其基因的突变进行修饰。然而,过度的色素沉着可能会影响微循环并导致贫血。
关键词: 黑色素沉着,疟疾,贫血症,β-地中海贫血,细胞溶质的钙离子,糖尿病
Current Medicinal Chemistry
Title:Eryptosis: Ally or Enemy
Volume: 24 Issue: 9
关键词: 黑色素沉着,疟疾,贫血症,β-地中海贫血,细胞溶质的钙离子,糖尿病
摘要: Prior to senescence, erythrocytes may experience injury, which compromises their integrity and thus triggers suicidal erythrocyte death or eryptosis. This mechanism is characterised by cell shrinkage, cell membrane blebbing, and cell membrane phospholipid scrambling after phosphatidylserine exposure on the cell surface that is identified by macrophages, which engulf and degrade the eryptotic cells. The term eryptosis also includes typical mechanisms, which contribute to the triggering of this process, such as oxidative stress, Ca2+ entry with an increase in cytosolic Ca2+ activity ([Ca ]i) and the activation of p38 kinase, which is a kinase expressed in human erythrocytes and activated after hyperosmotic shock. Enhanced eryptosis has been observed in several clinical conditions such as diabetes, renal insufficiency, haemolytic uremic syndrome, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anaemia, beta-thalassemia, glucose-6-phosphate dehydrogenase-(G6PD) deficiency, hereditary spherocytosis, paroxysmal nocturnal haemoglobinuria, Wilson's disease, myelodysplastic syndrome, and phosphate depletion. Therefore, eryptosis may be considered as a useful mechanism of removal of defective erythrocytes to prevent haemolysis. Moreover, the clearance of infected erythrocytes in diseases such as malaria may counteract parasitemia. Indeed it is known that sickle-cell trait, beta-thalassemia trait, glucose-6-phosphate dehydrogenase (G6PD)- deficiency and iron deficiency confer some protection against a severe course of malaria. Importantly, strategies to control Plasmodium infection by inducing eryptosis are not expected to generate resistance of the pathogen, as the proteins involved in suicidal death of the host cell are not encoded by the pathogen and thus cannot be modified by mutations of its genes. However, excessive eryptosis could compromise microcirculation and lead to anemia.
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Cite this article as:
Eryptosis: Ally or Enemy, Current Medicinal Chemistry 2017; 24 (9) . https://dx.doi.org/10.2174/0929867324666161118142425
DOI https://dx.doi.org/10.2174/0929867324666161118142425 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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