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红细胞衰老的分子机制。

Molecular mechanisms of erythrocyte aging.

作者信息

Hoehn Richard S, Jernigan Peter L, Chang Alex L, Edwards Michael J, Pritts Timothy A

出版信息

Biol Chem. 2015 Jun;396(6-7):621-31. doi: 10.1515/hsz-2014-0292.

Abstract

Anemia and hemorrhagic shock are leading causes of morbidity and mortality worldwide, and transfusion of human blood products is the ideal treatment for these conditions. As human erythrocytes age during storage in blood banks they undergo many biochemical and structural changes, termed the red blood cell 'storage lesion'. Specifically, ATP and pH levels decrease as metabolic end products, oxidative stress, cytokines, and cell-free hemoglobin increase. Also, membrane proteins and lipids undergo conformational and organizational changes that result in membrane loss, viscoelastic changes and microparticle formation. As a result, transfusion of aged blood is associated with a host of adverse consequences such as decreased tissue perfusion, increased risk of infection, and increased mortality. This review summarizes current research detailing the known parts of the erythrocyte storage lesion and their physiologic consequences.

摘要

贫血和失血性休克是全球发病和死亡的主要原因,输注人血制品是治疗这些病症的理想方法。随着人类红细胞在血库储存过程中老化,它们会发生许多生化和结构变化,称为红细胞“储存损伤”。具体而言,随着代谢终产物、氧化应激、细胞因子和游离血红蛋白增加,三磷酸腺苷(ATP)和pH值水平会降低。此外,膜蛋白和脂质会发生构象和组织变化,导致膜丢失、粘弹性变化和微粒形成。因此,输注老化血液会带来一系列不良后果,如组织灌注减少、感染风险增加和死亡率上升。本综述总结了当前的研究,详细阐述了红细胞储存损伤的已知部分及其生理后果。

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