Erythropoietin reduces storage lesions and decreases apoptosis indices in blood bank red blood cells

Peñuela, Oscar; Palomino, Fernando; Gómez, Lina Andrea

doi:10.1016/j.bjhh.2015.10.003

Cited by 2 publications

(1 citation statement)

References 30 publications

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“…Знания об этом могут способствовать разработке методов улучшения выживаемости эритроцитов при хранении и после переливания крови, а также целевому выбору эритроцитных взвесей или концентратов ОБЗОРЫ ПО КЛИНИЧЕСКОЙ ФАРМАКОЛОГИИ И ЛЕКАРСТВЕННОЙ ТЕРАПИИ 2019/17/3 эритроцитов и даже доноров для конкретных групп пациентов. В отдельных работах было высказано предположение, что эритроцит-содержащие компоненты крови с высоким содержанием гемоглобина следует переливать вместе с большим объемом крови [238]. Причем целесообразно подбирать компоненты с наименьшей экстернализацией фосфатидилсерина для пациентов с многократными переливаниями и для больных с выраженной анемией или удалить эритроциты, которые восприимчивы к стресс-индуцированному воздействию.…”

Section: эриптоз как элемент патогенеза анемииunclassified

Eryptosis (quasi-apoptosis) the human red blood cells. Its role in medicinal therapy

Vaschenko

Иванович²,

Vilyaninov

et al. 2019

Rev Clin Pharm Drug Ther

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In the course of circulation erythrocytes can test damages, 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 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, 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. Besides, adhesion of eryptosis erythrocytes to a vascular wall also can lead to microcirculation infringement.Thus, modern representations about eryptosis expand our knowledge about the programmed death of blood cells and is more directed to create new therapeutic schemes of treatment of patients.

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Section: эриптоз как элемент патогенеза анемииunclassified