{"title":"“Impact of peptidylarginine deiminase 4 (PAD4) deficiency in a fecal-induced peritonitis model of sepsis”: comment","authors":"Huimin Meng, Yongyan Han, Junli Yang, Pu Wang","doi":"10.1016/j.jtha.2025.06.032","DOIUrl":"10.1016/j.jtha.2025.06.032","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 10","pages":"Pages 3404-3405"},"PeriodicalIF":5.0,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
James B Wetmore, Chuanyu Kou, Nazleen F Khan, Irina Barash, G Brandon Atkins, Dena R Ramey, Nicholas S Roetker
{"title":"Major adverse thrombotic events and bleeding in stage 4 and 5 chronic kidney disease and dialysis-dependent end-stage kidney disease.","authors":"James B Wetmore, Chuanyu Kou, Nazleen F Khan, Irina Barash, G Brandon Atkins, Dena R Ramey, Nicholas S Roetker","doi":"10.1016/j.jtha.2025.08.025","DOIUrl":"10.1016/j.jtha.2025.08.025","url":null,"abstract":"<p><strong>Background: </strong>Balancing the risks of thrombotic and bleeding events in people with advanced kidney disease is a clinical challenge.</p><p><strong>Objectives: </strong>To estimate rates of major adverse thrombotic events (MATEs) and bleeding events in individuals with chronic kidney disease (CKD) stage 4 or 5 or with end-stage kidney disease receiving hemodialysis (HD) or peritoneal dialysis (PD).</p><p><strong>Methods: </strong>Using administrative claims from a 20% Medicare sample, Optum's deidentified Clinformatics Data Mart database, and the United States Renal Data System from 2016 to 2019, we identified individuals with CKD stages 4 or 5 and individuals with dialysis-dependent end-stage kidney disease. During follow-up (3 years maximum), we estimated incidence rates of MATEs (a composite of myocardial infarction, ischemic stroke, systemic embolism, deep vein thrombosis, pulmonary embolism, and critical limb ischemia events) and bleeding events (including major and clinically relevant nonmajor bleeding) using Poisson regression.</p><p><strong>Results: </strong>Among older adults insured by fee-for-service Medicare, incidence rates of MATEs for stages 4 and 5 CKD were 8.7 and 10.4 per 100 person-years, respectively; those for HD and PD were 13.5 and 14.3 per 100 person-years, respectively. Incidence rates of bleeding events were 13.8 (stage 4 CKD), 16.8 (stage 5 CKD), 21.7 (HD), and 20.2 (PD) per 100 person-years. Rates of MATEs and bleeding events in individuals with CKD insured by Medicare Advantage or commercial insurance followed similar patterns but were lower.</p><p><strong>Conclusion: </strong>Rates of MATEs and bleeding events increased with greater severity of kidney disease, illustrating the difficulty associated with balancing the management of these events in populations at high risk for both.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paola Colpani, Luciano Baronciani, Ilaria Mancini, Cristina Novembrino, Anna Lecchi, Giovanna Cozzi, Pasqualina De Leo, Massimo Boscolo Anzoletti, Silvia La Marca, Marco Boscarino, Maria Teresa Pagliari, Andrea Artoni, Flora Peyvandi
{"title":"Evaluation of different platelet-dependent von Willebrand factor activity assays to assess the in vivo inhibitory effect of caplacizumab on the von Willebrand factor-platelet interaction.","authors":"Paola Colpani, Luciano Baronciani, Ilaria Mancini, Cristina Novembrino, Anna Lecchi, Giovanna Cozzi, Pasqualina De Leo, Massimo Boscolo Anzoletti, Silvia La Marca, Marco Boscarino, Maria Teresa Pagliari, Andrea Artoni, Flora Peyvandi","doi":"10.1016/j.jtha.2025.08.020","DOIUrl":"10.1016/j.jtha.2025.08.020","url":null,"abstract":"<p><strong>Background: </strong>Caplacizumab, a humanized anti-von Willebrand factor (VWF) Nanobody, is used for immune-mediated thrombotic thrombocytopenic purpura (iTTP) treatment. Its binding to the VWF A1 domain inhibits VWF interaction with platelet glycoprotein (GP)Ib, counteracting microthrombosis and accelerating the normalization of the platelet count. In caplacizumab-treated patients with iTTP with bleeding episodes, measuring platelet-dependent VWF activity (VWF activity) is crucial for monitoring treatment with VWF concentrates. This activity, traditionally assessed by the VWF-ristocetin cofactor assay (VWF:RCo), nowadays could be evaluated with alternative methods as gain-of-function mutant GPIb binding assay (VWF:GPIbM), ristocetin-triggered GPIb binding assay (VWF:GPIbR), and monoclonal antibody binding-based VWF activity (VWF:Ab).</p><p><strong>Objectives: </strong>This study aimed to evaluate the capacity of 5 VWF activity assays to measure caplacizumab in vivo inhibitory effect on VWF-GPIb interaction.</p><p><strong>Methods: </strong>In total, 17 patients with iTTP treated effectively with caplacizumab, as demonstrated by normal platelet counts, were assessed by VWF activity using 5 commercially available assays. Three patients were further evaluated with the total thrombus analysis system (T-TAS).</p><p><strong>Results: </strong>Patients treated with caplacizumab showed no VWF activity using VWF:GPIbM and VWF:RCo assays. The VWF:Ab assay produced the highest values, while both VWF:GPIbR assays showed reduced VWF activity levels, although not to the extent of VWF:GPIbM and VWF:RCo. In patients analyzed by T-TAS no capillary occlusion was observed, indicating complete inhibition of the VWF-GPIb interaction by caplacizumab.</p><p><strong>Conclusion: </strong>The VWF:GPIbM and VWF:RCo appear to be the most suitable assays for monitoring VWF activity in patients with iTTP undergoing treatment with caplacizumab, as confirmed by T-TAS analysis. The VWF:GPIbR assays may be useful, but have a limited ability to detect caplacizumab's inhibition. The VWF:Ab assay is unsuitable for this purpose.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vincent R Lanting, Floris T M Bosch, Emily S L Martens, Pieter W Kamphuisen, Stefano Barco, Ramón Lecumberri, Hans-Martin Otten, Francesca Schieppati, Corrado Lodigiani, María Barca-Hernando, Elena Campello, Frederikus A Klok, Luis Jara-Palomares, Ettore Porreca, Harry R Büller, Nick van Es, Marcello Di Nisio
{"title":"Management of recurrent venous thromboembolism during anticoagulant treatment in patients with cancer: a prospective cohort study.","authors":"Vincent R Lanting, Floris T M Bosch, Emily S L Martens, Pieter W Kamphuisen, Stefano Barco, Ramón Lecumberri, Hans-Martin Otten, Francesca Schieppati, Corrado Lodigiani, María Barca-Hernando, Elena Campello, Frederikus A Klok, Luis Jara-Palomares, Ettore Porreca, Harry R Büller, Nick van Es, Marcello Di Nisio","doi":"10.1016/j.jtha.2025.08.022","DOIUrl":"10.1016/j.jtha.2025.08.022","url":null,"abstract":"<p><strong>Background: </strong>Recurrent venous thromboembolism (VTE) is a common complication in patients with cancer-associated VTE. Limited data are available on treatment, particularly in patients receiving direct oral anticoagulants (DOACs).</p><p><strong>Objectives: </strong>We aimed to evaluate current management strategies and outcomes in patients with cancer and recurrent VTE during treatment with low-molecular-weight heparin (LMWH) or DOACs.</p><p><strong>Methods: </strong>This was an international, prospective, observational cohort study. Patients were treated according to local practice, although the study protocol encouraged the use of a dose-escalation strategy in accordance with current clinical guidelines. Primary outcomes were second recurrent VTE and clinically relevant bleeding.</p><p><strong>Results: </strong>Between June 2020 and November 2024, 94 patients were enrolled, of whom 81 were included in the final analysis. At the time of recurrent VTE, 55% of patients were treated with a DOAC, 41% with therapeutic-dose LMWH, and 4% with maintenance-dose LMWH. Of DOAC-treated patients, 51% switched to supratherapeutic-dose LMWH, 42% to therapeutic-dose LMWH, and 7% received other treatments. Of LMWH-treated patients, 70% received dose escalation, 18% maintained the same dose, and 12% received other treatments. At the 3-month follow-up, 10% had developed a second recurrence, 12% clinically relevant bleeding, and 20% died. VTE incidence was similar between patients receiving dose escalation and those maintained on therapeutic doses, while clinically relevant bleeding was more frequent in the latter (6% vs 25%).</p><p><strong>Conclusion: </strong>The risk of second recurrent VTE was substantial despite two-thirds of patients receiving dose escalation. Bleeding was common regardless of treatment intensity, underscoring the challenges in this patient population.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wen Wang, Juping Zhai, Yao Wang, Xinyu Li, Jianfeng Yang, Zhen Weng, Yunxiao Zhao, Qingyu Wu, Bin Zuo, Yang He
{"title":"Integrin β<sub>3</sub> dysregulation impairs megakaryopoiesis and microparticle production via disrupting Rho-associated protein kinase-dependent cytoskeletal dynamics.","authors":"Wen Wang, Juping Zhai, Yao Wang, Xinyu Li, Jianfeng Yang, Zhen Weng, Yunxiao Zhao, Qingyu Wu, Bin Zuo, Yang He","doi":"10.1016/j.jtha.2025.08.021","DOIUrl":"10.1016/j.jtha.2025.08.021","url":null,"abstract":"<p><strong>Background: </strong>Megakaryocyte (MK) fragmentation into proplatelets (PPTs) and microparticles (megakaryocyte-derived microparticles [MKMPs]) is well established, yet the mechanisms underlying MKMP generation remain unclear.</p><p><strong>Objectives: </strong>This study aimed to investigate the role of integrin β<sub>3</sub> and cytoskeletal dynamics during megakaryopoiesis and explore potential therapeutic targets for thrombocytopenia.</p><p><strong>Methods: </strong>Proplatelet formation and MKMP release were evaluated both in vivo and in vitro under integrin β<sub>3</sub> receptor-impaired environment. The integrin activation and RhoA-associated kinase triggered signaling were analyzed.</p><p><strong>Results: </strong>In human MK cultures, we demonstrated that the anti-β<sub>3</sub> antibody SZ21 hyperactivated RhoA‒Rho-associated protein kinase (ROCK) signaling, stabilizing F-actin polymerization via LIM kinase/myosin light chain 2 phosphorylation and impairing both PPT and MKMP release. MKMP release depends on actin depolymerization, whereas PPT formation requires microtubule assembly and actomyosin contraction, revealing differential cytoskeletal regulation among megakaryocytic byproducts. Pharmacologic ROCK inhibition with Y27632 rescued these defects in vitro and accelerated platelet recovery in thrombocytopenic mice without compromising hemostasis.</p><p><strong>Conclusions: </strong>Our study reveals a novel dysregulation of the integrin β<sub>3</sub>-ROCK axis in immune-mediated MK dysfunction and suggests that targeting ROCK signaling or cytoskeletal dynamics may represent promising therapeutic strategies for thrombocytopenia and other disorders affecting platelet production.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thomas A J McKinnon, Yi Liu, Fan Gong, Alain Chion, Stephen Rothery, X Frank Zhang, Golzar Mobayen
{"title":"Significance of the amino acid at position 2561 in the C4 domain of von Willebrand factor.","authors":"Thomas A J McKinnon, Yi Liu, Fan Gong, Alain Chion, Stephen Rothery, X Frank Zhang, Golzar Mobayen","doi":"10.1016/j.jtha.2025.08.023","DOIUrl":"10.1016/j.jtha.2025.08.023","url":null,"abstract":"<p><strong>Background: </strong>The von Willebrand factor (VWF) Phe2561Tyr variant has been previously shown to exhibit gain-of-function-like activity and increase the risk of repeated myocardial infarction in patients aged <55 years. It was hypothesized that altered stem dynamics enhanced the responsiveness of the molecule to shear stress.</p><p><strong>Objectives: </strong>In this study, we investigated the evolutionary significance of the amino acid at position 2561 and functional impacts of variants at this site.</p><p><strong>Methods: </strong>Variants at 2561 identified by protein sequence alignments were generated by mutagenesis and expressed in HEK293T cells and function investigated using static and flow-based assays and biophysical methods.</p><p><strong>Results: </strong>Phe2561 was heavily conserved in mammals; however, nonmammals occupied the site with tyrosine, threonine, or serine. Recombinant expression of Phe2561Tyr/Thr/Ser showed no effects on expression, multimers, collagen or glycoprotein IIbIIIa binding, but Ser2561 and Thr2561 demonstrated enhanced binding to gain-of-function glycoprotein Ibα. While none of the variants, including Tyr2561, enhanced VWF-mediated platelet capture to collagen at 1500/s or 5000/s, the Tyr2561, Ser2561, and Thr2561 variants exhibited enhanced formation of rolling VWF-platelet aggregates, with Ser2561 demonstrating the greatest gain-of-function activity. Optical tweezer pulling experiments using VWF-D'CK dimers revealed altered unfolding properties of the Tyr, Thr, and Ser2561 protein and atomic force microscopy imaging of VWF dimeric stems demonstrated that Tyr, Thr, and Ser2561 favored a more open stem state, suggesting this is responsible for the enhanced response to shear stress.</p><p><strong>Conclusion: </strong>This study indicates that the amino acid at 2561 is crucial for modulating VWF function by helping to mediate stem dynamics.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Relieving platelet inhibition using a novel bispecific antibody: a novel approach for circumventing the platelet storage lesion.","authors":"Alyssa J Moroi, Cathy Paddock, Peter J Newman","doi":"10.1016/j.jtha.2025.08.018","DOIUrl":"10.1016/j.jtha.2025.08.018","url":null,"abstract":"<p><strong>Background: </strong>Human platelets undergo structural and functional deterioration during extracorporeal storage at either room or cold temperature, impairing their reactivity and diminishing their hemostatic effectiveness following transfusion. PECAM-1 is an inhibitory receptor on platelets that exerts its inhibitory effects via phosphorylation of tyrosine residues that lie within its cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs).</p><p><strong>Objectives: </strong>The purpose of this investigation was to attempt to restore platelet reactivity by impairing the inhibitory activity of PECAM-1.</p><p><strong>Methods: </strong>To counteract PECAM-1-mediated inhibition, we developed a novel bispecific tandem single-chain variable fragment that ligates the protein tyrosine phosphatase, CD148, with PECAM-1, promoting dephosphorylation of PECAM-1 ITIMs. We then analyzed the ability of this engineered tandem single-chain variable fragment (taFv 179) to improve adhesion and aggregation responses in vitro and under conditions of flow.</p><p><strong>Results: </strong>Addition of taFv 179 enhanced secretion, aggregation, and activation responses of both freshly isolated and stored platelets, particularly in response to weak agonists. taFv 179 also improved thrombus formation on collagen-coated surfaces under conditions of arterial flow.</p><p><strong>Conclusion: </strong>These findings demonstrate that enforced approximation of a phosphatase next to PECAM-1 ITIM tyrosine receptors is a novel strategy for enhancing the functionality of stored platelets, with potential implications for improving the effectiveness of platelet transfusion therapy.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Teagan Prouse, Alan E Mast, Vera Ignjatovic, Mirjana Kovac, Zsuzsanna Bereczky, Rinku Majumder
{"title":"Alternate functions of physiological anticoagulants.","authors":"Teagan Prouse, Alan E Mast, Vera Ignjatovic, Mirjana Kovac, Zsuzsanna Bereczky, Rinku Majumder","doi":"10.1016/j.jtha.2025.08.014","DOIUrl":"10.1016/j.jtha.2025.08.014","url":null,"abstract":"<p><p>The anticoagulant proteins antithrombin, protein C, protein S, and tissue factor pathway inhibitor are physiological regulators of the blood coagulation pathway and have complex roles in causing or modifying the severity of bleeding and clotting disorders. The anticoagulant activity, as well as alternative physiological functions, of these proteins also impact many other diseases beyond bleeding and clotting disorders. We searched PubMed for articles published between 2018 and early 2025 that pertained to alternative functions of these physiological anticoagulants in clinical disease and selected therapeutic applications in the following categories: cancer, cardiovascular disease, novel therapeutics, pregnancy health, inflammation and infection, blood-brain barrier protection, stroke, novel developments in thrombosis, and endothelial and platelet interactions. This review highlights recently identified physiological implications of antithrombin, protein C, protein S, and tissue factor pathway inhibitor functions that present an exciting therapeutic avenue for a diverse array of human diseases.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pia Larsson, Abigail McGovern, Volga Tarlac, Natasha M Setiabakti, Louis Parker, Stephen H Cody, Juan Nunez-Iglesias, Lars Faxälv, Lisa Prahl Wittberg, Justin R Hamilton, Niklas Boknäs
{"title":"Confining thrombus morphospace through targeted inhibition of platelet mechanosensory signaling.","authors":"Pia Larsson, Abigail McGovern, Volga Tarlac, Natasha M Setiabakti, Louis Parker, Stephen H Cody, Juan Nunez-Iglesias, Lars Faxälv, Lisa Prahl Wittberg, Justin R Hamilton, Niklas Boknäs","doi":"10.1016/j.jtha.2025.08.013","DOIUrl":"https://doi.org/10.1016/j.jtha.2025.08.013","url":null,"abstract":"<p><strong>Background: </strong>While current antiplatelets protect against thrombosis, their clinical utility is limited by an elevated risk of bleeding.</p><p><strong>Objectives: </strong>To understand how structure-function relations in the hemostatic system may be leveraged into improved risk/benefit ratios for antiplatelet therapies.</p><p><strong>Methods: </strong>We developed a deep learning-based framework to track the activities of large numbers of platelets in vivo, enabling a detailed comparative assessment of the effects of therapeutic interventions on the evolving structural hierarchy of the hemostatic response.</p><p><strong>Results: </strong>Unlike conventional antiplatelets targeting paracrine signaling, selective pharmaceutical inhibition of platelet mechanosensory signaling (iPMS) via PI3KC2α preserved the initial build-up of thrombi following vascular injury to high-flow mesenteric veins. However, as this burst of hemostatic activity subsided, iPMS caused localized reductions of platelet [Ca<sup>2+</sup>]<sub>i</sub> in shear-exposed peripheral thrombus subregions, inhibiting the formation of platelet clusters capable of withstanding the drag forces of the blood flow. As a consequence, platelets in these subregions detached, became elongated and/or slided along the thrombus surface. On a macrostructural level, this selective destabilization prevented sustained physical expansion of thrombi outside the perimeters of vascular injuries, while preserving platelet packing density in thrombus subregions close to vascular injuries.</p><p><strong>Conclusions: </strong>Collectively, our results highlight platelet mechanosensory signaling as a significant driver of sustained platelet population growth after the initial agonist-driven phase of thrombus expansion. We show that pharmaceutical targeting of this pathway enforced the convergence of thrombus growth trajectories towards a rheologically favourable setpoint, without compromising the structural integrity of thrombus subregions that are critical for hemostasis.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}