ArticleResearch and practice in thrombosis and haemostasis2023
Platelets of COVID-19 patients display mitochondrial dysfunction, oxidative stress, and energy metabolism failure compatible with cell death.
Article in Research and practice in thrombosis and haemostasis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- Dysregulated metabolic homeostasis as a unifying death mechanism underlying the diverse clinical manifestations of COVID-19: insights from a retrospective analysis of sequential blood variables.Frontiers in medicine · 2026Article
- Hyperinflammation by Human Macrophages Induced by SARS-CoV-2 Anti-Spike IgG Is Dependent on Glucose and Fatty Acid Metabolism.European journal of immunology · 2025Article
- Toll-like Receptor 7 Deficiency Attenuates Platelet Dysfunction in Sepsis.Biomolecules · 2025Article
- GPER in metabolic homeostasis and disease: molecular mechanisms, nutritional regulation, and therapeutic potential.Journal of translational medicine · 2025Review
- Differential platelet protein release profiles in community-acquired pneumonia and COVID-19.ERJ open research · 2025Article
- The protein interaction of mitochondrial transcription factors A and B2 is associated with 30-day survival in critical COVID-19.Frontiers in immunology · 2025Article
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Alterations in platelet function have been implicated in the pathophysiology of COVID-19 since the beginning of the pandemic. While early reports linked hyperactivated platelets to thromboembolic events in COVID-19, subsequent investigations demonstrated hyporeactive platelets with a procoagulant phenotype. Mitochondria are important for energy metabolism and the function of platelets. Objectives: Here, we sought to map the energy metabolism of platelets in a cohort of noncritically ill COVID-19 patients and assess platelet mitochondrial function, activation status, and responsiveness to external stimuli. Methods: We enrolled hospitalized COVID-19 patients and controls between October 2020 and December 2021. Platelets function and metabolism was analyzed by flow cytometry, metabolomics, glucose fluxomics, electron and fluorescence microscopy and western blot. Results: Platelets from COVID-19 patients showed increased phosphatidylserine externalization indicating a procoagulant phenotype and hyporeactivity to Conclusion: These data link energy metabolism failure in platelets from COVID-19 patients with a prothrombotic platelet phenotype with features matching cell death.
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