Research progress on mitochondria in platelet storage
10.13303/j.cjbt.issn.1004-549x.2026.06.016
- VernacularTitle:线粒体在血小板储存中的研究进展
- Author:
Yu PENG
1
;
Hongwei ZHANG
2
Author Information
1. Department of Laboratory Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China; Department of Blood Transfusion, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
2. Department of Blood Transfusion, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
- Publication Type:Journal Article
- Keywords:
platelet storage lesions;
platelet protection;
transfusion medicine
- From:
Chinese Journal of Blood Transfusion
2026;39(6):809-817
- CountryChina
- Language:Chinese
-
Abstract:
As the center of energy metabolism and a key hub of intracellular signal transduction in platelets, platelet mitochondria play a core role in maintaining platelet activation, apoptosis, and functional homeostasis. Mitochondria not only provide approximately 90% of platelet ATP through oxidative phosphorylation (OXPHOS), but also deeply participate in platelet activation, secretion, aggregation, and apoptosis-like programmed death by regulating reactive oxygen species (ROS) generation, mitochondrial membrane potential (ΔΨm), and the opening of the mitochondrial permeability transition pore (mPTP). During platelet storage, mitochondrial dysfunction is a core mechanism underlying platelet storage lesions. Therefore, targeting mitochondrial function protection—such as through supplementation of metabolic substrates, application of mitochondria-targeted antioxidants, or mPTP inhibitors—holds promise as a novel intervention strategy to ameliorate platelet storage lesions, prolong platelet survival in vivo, and reduce adverse transfusion reactions.
