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D. Stefanoni et al.
Discussion
Over the past two decades, animal models have helped to identify potential mechanisms critical to RBC storage biology and transfusion outcomes. Murine and canine models of RBC storage and transfusion were critical in identifying (i) etiological contributions to transfusion- related acute lung injury, including the two-hit model;39 (ii) the impact of storage duration on mortality,21 and (iii)
the role that iron overload plays in increasing the risk of septic complications.19 These models have limited genetic variability and a more homogeneous exposome than humans. This controlled strain-specific heterogeneity of genetic background in rodent models enables mechanistic studies to identify genetic and metabolic contributors to RBC storage quality and the post-transfusion perform- ance of the RBC.17,18 In addition, animal models can be modified in a controlled fashion to allow for selective
Figure 6. Species- and storage time-specific metabolic changes in Rhesus macaques and human red blood cells: focus on acyl-carnitines, free fatty acid metab- olism, and lipid peroxidation products. Data for Rhesus macaques are shown in green, those for humans are represented in red.
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