ReviewInternational journal of molecular sciences2021
Carboxypeptidase U (CPU, TAFIa, CPB2) in Thromboembolic Disease: What Do We Know Three Decades after Its Discovery?
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Emerging strategies in venous thromboembolism: a narrative review of pharmacological innovations.Thrombosis journal · 2026Review
- Comparative molecular dynamics mapping of metallocarboxypeptidase-peptide interfaces reveals potential hotspots that inspire novel inhibitor design.Scientific reports · 2026Article
- Association of Carboxypeptidase B2 Gene Polymorphisms With Graft Loss in Kidney Transplantation.Transplantation direct · 2026Article
- Management of cancer-associated venous thromboembolism: Perspectives on optimizing current therapeutics with a focus on factor XI inhibition.Journal of thrombosis and thrombolysis · 2025Review
- Recent Pathophysiological Insights Are Advancing the Treatment of Venous Thromboembolism.JACC. Basic to translational science · 2025Review
- Comparison of the proteomic landscape in experimental ischemia reperfusion with versus without ischemic preconditioning.Scientific reports · 2025Article
- Systemic Inflammatory Response Syndrome, Thromboinflammation, and Septic Shock in Fetuses and Neonates.International journal of molecular sciences · 2025Review
- Targeting Fibrinolytic Inhibition for Venous Thromboembolism Treatment: Overview of an Emerging Therapeutic Approach.Circulation · 2024Review
- Cutting-Edge Techniques and Drugs for the Treatment of Pulmonary Embolism: Current Knowledge and Future Perspectives.Journal of clinical medicine · 2024Review
- Profibrinolytic effects of rivaroxaban are mediated by thrombin-activatable fibrinolysis inhibitor and are attenuated by a naturally occurring stabilizing mutation in enzyme.Journal of thrombosis and thrombolysis · 2023Article
- Association between TAFI and PAI-1 polymorphisms with biochemical and hemostatic parameters in polycystic ovary syndrome.Archives of gynecology and obstetrics · 2023Article
- SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock.Frontiers in physiology · 2023Review
- Activation of the Carboxypeptidase U (CPU, TAFIa, CPB2) System in Patients with SARS-CoV-2 Infection Could Contribute to COVID-19 Hypofibrinolytic State and Disease Severity Prognosis.Journal of clinical medicine · 2022Article
- Efficacy and Mechanism of Buyang Huanwu Decoction in Patients With Ischemic Heart Failure: A Randomized, Double-Blind, Placebo-Controlled Trial Combined With Proteomic Analysis.Frontiers in pharmacology · 2022Article
- Pleiotropic Effects of Atorvastatin Result in a Downregulation of the Carboxypeptidase U System (CPU, TAFIa, CPB2) in a Mouse Model of Advanced Atherosclerosis.Pharmaceutics · 2021Article
- Thrombin Activatable Fibrinolysis Inhibitor (TAFI): An Updated Narrative Review.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Procarboxypeptidase U (proCPU, TAFI, proCPB2) is a basic carboxypeptidase zymogen that is converted by thrombin(-thrombomodulin) or plasmin into the active carboxypeptidase U (CPU, TAFIa, CPB2), a potent attenuator of fibrinolysis. As CPU forms a molecular link between coagulation and fibrinolysis, the development of CPU inhibitors as profibrinolytic agents constitutes an attractive new concept to improve endogenous fibrinolysis or to increase the efficacy of thrombolytic therapy in thromboembolic diseases. Furthermore, extensive research has been conducted on the in vivo role of CPU in (the acute phase of) thromboembolic disease, as well as on the hypothesis that high proCPU levels and the Thr/Ile325 polymorphism may cause a thrombotic predisposition. In this paper, an overview is given of the methods available for measuring proCPU, CPU, and inactivated CPU (CPUi), together with a summary of the clinical data generated so far, ranging from the current knowledge on proCPU concentrations and polymorphisms as potential thromboembolic risk factors to the positioning of different CPU forms (proCPU, CPU, and CPUi) as diagnostic markers for thromboembolic disease, and the potential benefit of pharmacological inhibition of the CPU pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.