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Updated: May 29, 2026

LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
Published on: April 4, 2016
Platelet Mitochondria: A Promising Target for Antiplatelet Therapy
Yan-Zhu Yao1, Tong Yin1, Yong-Ming Yao2
1Institute of Geriatrics, Beijing Key Laboratory of Aging and Geriatrics, National Clinical Research Center for Geriatric Diseases, Second Medical Center of the Chinese PLA General Hospital, Beijing, China.
Significance:
Platelet mitochondria drive platelet activation and thrombosis by fueling energy demands via metabolic reprogramming, regulating calcium-mediated procoagulant signaling, and maintaining functional integrity through quality control mechanisms. Current antiplatelet agents, including P2Y12 antagonists, cyclooxygenase-1 inhibitors, glycoprotein IIb/IIIa blockers, and protease-activated receptor-1 antagonists, effectively prevent thrombosis but increase bleeding risk, underscoring the need for metabolism-targeting strategies.
Recent Advances:
Here, we summarize key platelet mitochondrial mechanisms driving platelet activation: metabolic reprogramming through oxidative phosphorylation (OXPHOS)-to-glycolysis shifts, calcium flux mediated by the mitochondrial calcium uniporter controlling coagulation, quality control through dynamics and mitophagy, and mitochondrial genome (mtDNA) regulation linked to relevant diseases.
Critical Issues:
The variable role of OXPHOS in thrombosis remains incompletely understood. Metabolic flexibility complicates therapeutic intervention, while the cytotoxic effects of mitochondrial modulators and technical limitations in the quantification of circulating mtDNA present significant translational challenges.
Future Directions:
Development of therapies based on mitochondria-targeted antioxidants and metabolic enzyme modulators is proposed as a promising antiplatelet strategy. Transplantation of platelet-derived mitochondria and standardized detection of mtDNA warrant further exploration for thrombotic diseases. Antioxid. Redox Signal. 45, 265-292.
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