Highlight
Sepsis-induced mitochondrial dysfunction impairs platelet respiration and enhances platelet activation. Mitochondria-targeted antioxidant MitoTEMPO reverses these effects in vitro, indicating the critical role of mitochondrial reactive oxygen species (ROS) in platelet hyperactivation. This study suggests mitochondrial ROS scavengers as potential adjunct therapies to prevent sepsis-mediated organ damage.
Study Background
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