Molecular mechanisms of erythrocyte aging

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.

Figure 1

Light microscopy images demonstrating changes in human erythrocyte morphology during storage. pRBCs were stored in AS-3 at 4°C. Over time, erythrocytes develop loss of biconcave disc shape, subsequently changing to echinocytes and spherocytes. Images adopted from Makley et al. (2010b).