Utilization of mitochondrial-targeted small molecules in protecting stored platelets against storage lesions

Abstract

Platelet transfusion is frequently applied to control and prevent bleeding under many clinical settings. However, the current storage strategy limits the collected platelets to a shelf life of only 5–7 days due to platelet storage lesion (PSL). To date, mitochondria are reported to play a pivotal role in platelet energy metabolism, platelet activation and platelet apoptosis. In addition, the development of PSL is closely associated with oxidative stress and mitochondrial dysfunction. Hence, efforts to preserve mitochondrial function against oxidative stress may potentially curtail PSL and extend the shelf life of platelet concentrates (PCs). The research summarized in this review shows that many small molecules have a beneficial effect on stored platelets, and we believe that addition of small molecules for mitochondrial targeted intervention may be an effective approach in mitigating PSL and thereby extend the shelf life of PCs.