Platelets, crucial components of blood, play a vital role in hemostasis and clinical treatments. However, current platelet storage methods at 22 +/- 2 degrees C face significant limitations, including a short shelf life (5-7 days), high risk of bacterial contamination, and progressive accumulation of metabolites such as lactic acid during prolonged storage. These issues impair transfusion efficacy and severely restrict the clinical utility of platelets. In contrast, cold storage at 4 degrees C offers potential advantages: it extends platelet shelf life, reduces bacterial contamination risks, minimizes metabolite accumulation, and better preserves platelet hemostatic function. Mitochondria, as essential organelles in platelets, are central to energy metabolism, activation, adenosine triphosphate production, and regulation of cellular processes. They are of great significance for maintaining platelet physiological function and biological activity. This review examines the role of mitochondria in refrigerated platelet storage, focusing on their impact on energy metabolism, apoptosis, and post-transfusion clearance. Additionally, we discuss mitochondrial-targeted intervention strategies and future research directions to optimize platelet storage methods and enhance clinical transfusion outcomes.