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Studies of stored RBCs in blood bank conditions also reported the recruitment of Prx2, CAT and GPx to the RBC membrane due to OS modifications resulting from the metabolic stress of long-term erythrocyte storage [93, 97]

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Together, increased intraplaque cellular death and dysfunctional efferocytosis as a result of G6PD-d may accelerate plaque growth, necrotic core formation and the development of an inflammatory plaque microenvironment 106,107 (Fig