Thrombosis research最新文献

{"title":"Activation of the pentose phosphate pathway mitigates platelet storage lesions and improves platelet preservation quality","authors":"Liujun Guo ,&nbsp;Chengrui Qian ,&nbsp;Chengyan Gao ,&nbsp;Hasiyati Heililahong ,&nbsp;Min Xin ,&nbsp;Lei Hang ,&nbsp;Can Lou ,&nbsp;Jiaming Li ,&nbsp;Xuefeng Wang ,&nbsp;Jing Dai ,&nbsp;Xuemei Fan ,&nbsp;Xiaohong Cai","doi":"10.1016/j.thromres.2025.109377","DOIUrl":"10.1016/j.thromres.2025.109377","url":null,"abstract":"<div><h3>Background</h3><div>Platelet storage lesions (PSLs) impact platelet lifespan and transfusion quality. This study explores platelet storage metabolism for potential interventions.</div></div><div><h3>Methods</h3><div>Samples were collected on days 1, 3, and 5 for untargeted metabolomics analysis to identify metabolites that differ with storage time and potential metabolic pathways. The activities of glucose-6-phosphate dehydrogenase (G6PD) and cyclooxygenase-1 (COX-1) in platelets during storage were measured. Meanwhile, flow cytometry was used to assess changes in apoptosis and mitochondrial function of stored platelets treated with either a G6PD inhibitor, a G6PD activator, or a COX-1 inhibitor. Platelet aggregation was used to evaluate platelet function. Megakaryocyte/platelet-specific <em>G6pd</em> knockout mice were used to assess the role of G6PD in PSLs.</div></div><div><h3>Results</h3><div>The pentose phosphate pathway (PPP), arachidonic acid metabolism, and linoleic acid metabolism were enriched during storage. A total of 4832 platelet metabolites and 6468 plasma metabolites were identified, with 44 and 108 showing nominally significant changes respectively. An increase in G6PD activity was observed at the early stages. Inhibiting G6PD with G6PDi-1 damages mitochondria, increases phosphatidylserine externalization, and impairs platelet aggregation. Mouse <em>G6pd</em>^−/− platelets exhibited increased PSLs. Activation of G6PD with AG1 reduces mitochondrial reactive oxygen species (mtROS) and phosphatidylserine externalization while enhancing platelet aggregation. Additionally, although COX-1 activity in the arachidonic acid metabolism pathway increases at the early stage, its inhibition by the COX-1 inhibitor aspirin does not significantly alter PSL-related indicators.</div></div><div><h3>Conclusion</h3><div>The pentose phosphate pathway maintains platelet mitochondrial function via G6PD regulation, making G6PD a critical target for reducing PSLs.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109377"},"PeriodicalIF":3.7,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144272603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to letter to the editor","authors":"Ting Wei Teo ,&nbsp;Sarah Ming Li Tan ,&nbsp;Pipin Kojodjojo ,&nbsp;Yinghao Lim","doi":"10.1016/j.thromres.2025.109373","DOIUrl":"10.1016/j.thromres.2025.109373","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109373"},"PeriodicalIF":3.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critique and advice of a multicenter mechanical thrombectomy registry in intermediate-risk PE","authors":"Shifei He","doi":"10.1016/j.thromres.2025.109374","DOIUrl":"10.1016/j.thromres.2025.109374","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"253 ","pages":"Article 109374"},"PeriodicalIF":3.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treating the mind and body: implementation of a psychosocial wellbeing assessment in the deep vein thrombosis clinic","authors":"Emma Gee,&nbsp;Victoria Speed,&nbsp;Philip Alexander,&nbsp;Simon Guppy,&nbsp;Jig Patel,&nbsp;Sinead Duffy,&nbsp;Rachel Clapham,&nbsp;Roopen Arya","doi":"10.1016/j.thromres.2025.109360","DOIUrl":"10.1016/j.thromres.2025.109360","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109360"},"PeriodicalIF":3.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of exercise-based rehabilitation on objective physical activity levels in patients with persistent dyspnoea following pulmonary embolism","authors":"Stacey Haukeland-Parker ,&nbsp;Øyvind Jervan ,&nbsp;Waleed Ghanima ,&nbsp;Martijn A. Spruit ,&nbsp;Aliaksandr Hubin ,&nbsp;Mazdak Tavoly ,&nbsp;Jostein Gleditsch ,&nbsp;Trude Støver ,&nbsp;Knut Stavem ,&nbsp;Hege Hølmo Johannessen","doi":"10.1016/j.thromres.2025.109362","DOIUrl":"10.1016/j.thromres.2025.109362","url":null,"abstract":"<div><h3>Background</h3><div>Rehabilitation improves exercise capacity following pulmonary embolism (PE), but it is unclear whether this improvement is transferred into increased physical activity.</div><div><strong>Objectives.</strong></div><div>To explore the effect of exercise-based rehabilitation on objective measures of physical activity in patients with persistent dyspnoea following PE compared to standard care.</div></div><div><h3>Methods</h3><div>This pre-planned substudy compared an eight-week exercise-based rehabilitation program to usual care. Number of steps per day and time spent in sedentary, low, moderate and vigorous physical activity (in number of metabolic equivalent of tasks) were measured for seven consecutive days at baseline prior to intervention start and at post-intervention using accelerometery. Data were analysed with a mixed-effect generalised linear model.</div></div><div><h3>Results</h3><div>Complete data was provided by 48 patients at both timepoints (mean age 58 years, 54 % men) with 54 % randomised to rehabilitation. There were no significant differences between groups at baseline. The majority of time (717 min per day) was spent in sedentary activity and mean number of steps per day was 6701. At post-intervention, there were no significant differences between groups in any of the objectively measured physical activity parameters (<em>p</em> &gt; 0.05).</div></div><div><h3>Conclusion</h3><div>In this cohort, exercise-based rehabilitation following PE did not change daily physical activity levels compared to usual care control group.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109362"},"PeriodicalIF":3.7,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144222941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leukadherin-1 mitigates disseminated intravascular coagulation in acute pancreatitis by suppressing necroptosis","authors":"Zhongjie Yi ,&nbsp;Xueming Xu ,&nbsp;Xingyu Xiang ,&nbsp;Jinyuan Chang ,&nbsp;Jie Shi ,&nbsp;Yongjun Wang","doi":"10.1016/j.thromres.2025.109363","DOIUrl":"10.1016/j.thromres.2025.109363","url":null,"abstract":"<div><div>Disseminated intravascular coagulation (DIC) is a fatal complication of acute pancreatitis (AP), leading to multiple organ dysfunction syndrome (MODS), but its pathogenic mechanism is poorly understood. Here, we identify Leukadherin-1 (LA-1) as a potential therapeutic agent against AP-associated DIC. LA-1 effectively attenuated DIC progression by suppressing tissue factor (TF) release from necroptotic macrophages, achieved through inhibition of RIPK1 phosphorylation at Ser166—a critical step in necroptosis signaling pathways. Additionally, LA-1 inhibited necroptosis in pancreatic acinar cells, potentially disrupting macrophage necroptosis. These findings propose a novel approach to targeting the interplay between necroptosis and coagulation and provides valuable insights into potential therapeutic strategies for managing coagulation disorders associated with AP, thus alleviates the burden of this debilitating condition.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109363"},"PeriodicalIF":3.7,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of warfarin treatment in patients with antiphospholipid syndrome and falsely high INR at point-of-care-testing","authors":"Jørn Dalsgaard Nielsen ,&nbsp;Thomas Steffen Hermann ,&nbsp;Konstantinos Dimopoulos ,&nbsp;Anne Storgaard Nørskov","doi":"10.1016/j.thromres.2025.109361","DOIUrl":"10.1016/j.thromres.2025.109361","url":null,"abstract":"<div><h3>Background</h3><div>The standard of care for thrombotic antiphospholipid syndrome (APS) is anticoagulation with vitamin K antagonists (VKA). Several studies have indicated that lupus anticoagulant (LA) can interfere with the international normalized ratio (INR) results obtained by point-of-care testing (POCT) devices. A subset of patients with APS has clinically significant systematic differences between POCT INR and plasma INR (P-INR) measured in the hospital laboratory.</div></div><div><h3>Objectives</h3><div>We aimed to investigate a potential correlation between POCT INR (CoaguChek, Roche Diagnostics) and P-INR in these patients.</div></div><div><h3>Materials and methods</h3><div>In our anticoagulation clinic, we compared 363 paired CoaguChek-INR (CC-INR) with P-INR results using Owren's method from 37 patients with APS receiving self-managed VKA. Each patient had a minimum of three paired measurements of CC-INR and P-INR and a median CC-INR/P-INR ratio &gt; 1.20.</div></div><div><h3>Results</h3><div>In all patients, we found a strong linear correlation between CC-INR and P-INR (median R²: 0.89; IQR: 0.78–0.94). Each patient had their own characteristic regression line from which CC-INR could be converted to P-INR. Thirty-four patients continued with self-managed treatment and the use of a conversion table. However, 3 patients had to switch to INR control in the anticoagulation clinic, as the upper limit of their therapeutic CC-INR interval exceeded the maximum (INR: 8.0) on their CoaguChek device.</div></div><div><h3>Conclusions</h3><div>In a subset of patients with APS who, during self-managed VKA therapy, had persistently higher POCT INR than P-INR, the majority could continue with self-managed therapy using a conversion table, as the falsely elevated POCT INR values <!--> <!-->were linearly correlated to P-INR.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109361"},"PeriodicalIF":3.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144189892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All-cause mortality after major gastrointestinal bleeding among patients receiving direct oral anticoagulants: a systematic review and meta-analysis","authors":"Nicholas L.J. Chornenki ,&nbsp;Roupen Odabashian ,&nbsp;Marc Carrier ,&nbsp;Faizan Khan ,&nbsp;Jenneke Lenteejens ,&nbsp;Fabian Stucki ,&nbsp;Tzu-Fei Wang ,&nbsp;Tobias Tritschler ,&nbsp;Deborah M. Siegal","doi":"10.1016/j.thromres.2025.109352","DOIUrl":"10.1016/j.thromres.2025.109352","url":null,"abstract":"<div><h3>Background</h3><div>Although gastrointestinal (GI) bleeding represents the single most frequent site of anticoagulant-related major bleeding, outcomes after major GI bleeding including mortality are not well characterized and severity may be underappreciated. We aimed to determine 30-day all-cause mortality in adults with major GI bleeding on a direct oral anticoagulant (DOAC).</div></div><div><h3>Methods</h3><div>We searched MEDLINE, EMBASE, and Cochrane CENTRAL from inception to May 9, 2024 for randomized controlled trials and cohort studies that reported 30-day all-cause mortality after major GI bleeding in adults treated with a DOAC for venous thromboembolism or atrial fibrillation. Risk of bias was assessed using a modified QUIPS tool for prognostic studies. 30-day all-cause mortality was calculated using the random-effects inverse-variance method.</div></div><div><h3>Results</h3><div>We included 20 studies comprising 3987 DOAC-treated patients with major GI bleeds. The pooled estimate of 30-day all-cause mortality was 8.4 % (95 % confidence interval [CI], 4.9–12.5; I² = 83 %). In subgroup analyses, 30-day all-cause mortality was 10.3 % (95 % CI, 6.5–14.7; I² = 24 %) in prospective studies (9 studies, 675 major GI bleeds), 7.3 % (95 % CI, 2.2–14.4; I² = 90 %) in retrospective studies (11 studies, 3312 major GI bleeds), 12.9 % (95 % CI, 6.3–21.1; I² = 44 %) in considered at high risk of bias (9 studies, 387 major GI bleeds), and 6.1 % (95 % CI, 2.9–10.1; I² = 89 %) in those at low risk of bias (10 studies, 3562 major GI bleeds).</div></div><div><h3>Conclusion</h3><div>DOAC-related major GI bleeding appears to be associated with significant 30-day all-cause mortality. Further research is needed regarding the causes and contributors to mortality in this population to identify patients at high risk and develop mitigation strategies.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109352"},"PeriodicalIF":3.7,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Performance of new 2023 ACR/EULAR antiphospholipid syndrome classification criteria in young patients admitted for pulmonary embolism","authors":"Dalil Bouzid ,&nbsp;Diane Rouzaud ,&nbsp;Julien Rio ,&nbsp;Raphael Borie ,&nbsp;Christophe Choquet ,&nbsp;Gregory Ducrocq ,&nbsp;Jean-Francois Alexandra ,&nbsp;Antoine Dossier ,&nbsp;Thomas Papo ,&nbsp;Arthur Mageau ,&nbsp;Karim Sacre","doi":"10.1016/j.thromres.2025.109359","DOIUrl":"10.1016/j.thromres.2025.109359","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"252 ","pages":"Article 109359"},"PeriodicalIF":3.7,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of inflammation and proinflammatory proteins in coagulopathy during venovenous extracorporeal membrane oxygenation","authors":"Ya Wang ,&nbsp;Huadong Sun ,&nbsp;Jie Zhang ,&nbsp;Xiaowen Xie ,&nbsp;Yuheng Yu ,&nbsp;Zhenting Liang ,&nbsp;Weiyan Ye ,&nbsp;Zitao Zeng ,&nbsp;Xinyi Luo ,&nbsp;Dongdong Liu ,&nbsp;Yin Xi ,&nbsp;Rong Zhang ,&nbsp;Chun Yang ,&nbsp;Liang Zhou ,&nbsp;Manshu Li ,&nbsp;Jieyi Pan ,&nbsp;Zhiheng Xu ,&nbsp;Ling Sang ,&nbsp;Yuanda Xu ,&nbsp;Weiqun He ,&nbsp;Yonghao Xu","doi":"10.1016/j.thromres.2025.109358","DOIUrl":"10.1016/j.thromres.2025.109358","url":null,"abstract":"<div><h3>Background</h3><div>Coagulopathy frequently complicates venovenous extracorporeal membrane oxygenation (VV ECMO) procedures, yet its underlying mechanism remains elusive. This retrospective study aimed to identify factors contributing to coagulopathy during VV ECMO by analyzing clinical data and employing proteomic approaches. A prospective cohort was also examined for validation.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed clinical data from 51 patients undergoing VV ECMO between January 2015 and April 2021, categorizing them into coagulopathy(<em>n</em> = 21), defined by elevated levels of D-dimer and decreased fibrinogen in plasma that were reversible by circuit exchange, and non-coagulopathy(<em>n</em> = 30) groups. Plasma samples collected on days 0–2(D1), days 3–5(D4), and days 6–8(D7) were subjected to proteomics and Luminex assay. Additionally, oxygenator fiber samples were collected from a prospective cohort between May 2022 and August 2022 for scanning electron microscopy.</div></div><div><h3>Results</h3><div>Inflammation emerged as a pivotal factor in coagulopathy development during VV ECMO, as evidenced by elevated interleukin-6 levels on D1 and increased leukocyte and neutrophil counts on D4. Proteomics analysis identified a significant elevation of S100A8 and S100A9 in the plasma of coagulopathy patients throughout VV ECMO, findings confirmed by Luminex assay. In the prospective cohort, thrombosis and leukocyte accumulation were observed on oxygenator fibers from coagulopathy patients, along with elevated levels of S100A8 and S100A9 in plasma.</div></div><div><h3>Conclusions</h3><div>Coagulopathy during VV ECMO is associated with heightened levels of proinflammatory proteins S100A8 and S100A9 in plasma, accompanied by leukocyte accumulation on oxygenator fibers. These findings emphasize the potential therapeutic target against coagulopathy during VV ECMO.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"251 ","pages":"Article 109358"},"PeriodicalIF":3.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}