ArticlePlatelets2019
Auranofin, a thioredoxin reductase inhibitor, causes platelet death through calcium overload.
Article in Platelets, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Monitoring in real time and far-red imaging of HNature chemical biology · 2026Article
- Investigating the Synergistic Effect of the Cannabis Extract PHEC-66 and Chemotherapeutic Agents on Human Melanoma Cells.International journal of molecular sciences · 2026Article
- The zinc finger domains of PARP-1 are selectively and potently inhibited by the Au(I)-based drugs sodium aurothiomalate and aurothioglucose.FEBS letters · 2025Article
- Auranofin as a Novel Anticancer Drug for Anaplastic Thyroid Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- NINJ1 Regulates Platelet Activation and PANoptosis in Septic Disseminated Intravascular Coagulation.International journal of molecular sciences · 2023Article
- Speciation Analysis Highlights the Interactions of Auranofin with the Cytoskeleton Proteins of Lung Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The Thioredoxin System of Mammalian Cells and Its Modulators.Biomedicines · 2022Review
- Thioredoxin-dependent system. Application of inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2021Review
- Thrombocytopathies: Not Just Aggregation Defects-The Clinical Relevance of Procoagulant Platelets.Journal of clinical medicine · 2021Review
- Auranofin Mediates Mitochondrial Dysregulation and Inflammatory Cell Death in Human Retinal Pigment Epithelial Cells: Implications of Retinal Neurodegenerative Diseases.Frontiers in neuroscience · 2019Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelets are central to normal hemostasis and must be tightly controlled to prevent thrombosis. However, drug treatments that also affect platelets could lead to unwanted side effects on hemostasis or thrombosis. In this study, the effect of auranofin on platelets was tested. Auranofin, a gold-based thioredoxin reductase (TRXR) inhibitor, has been previously used in arthritis. Recently, auranofin and other inhibitors of the thioredoxin system have been proposed as novel anti-cancer therapies. TRXR is an important part of the antioxidant defenses in many cells that maintain intracellular proteins in their reduced state. TRXR activity in platelets could be completely inhibited by auranofin. Auranofin-treated platelets showed several features of cell death, including the inability to aggregate in response to thrombin, leakage of cytosolic lactate dehydrogenase, and surface exposure of procoagulant phosphatidylserine. Auranofin increased platelet reactive oxygen species production and intracellular calcium concentration. DTT, a sulfydyl reducing agent, and BAPTA-AM, which chelates intracellular calcium, prevented auranofin-induced phosphatidylserine exposure. These data suggest that TRXR is an important part of the platelet antioxidant defense. TRXR inhibition by auranofin triggers oxidative stress and disrupts intracellular calcium homeostasis, leading to platelet necrosis. The use of auranofin or other TRXR inhibitors could therefore lead to unwanted side effects.
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