Platelets最新文献

{"title":"Dornhorst's model revisited: an error identified in the equation for platelet survival.","authors":"Woo Young Shin, Kyeong Deok Kim, Keon-Young Lee","doi":"10.1080/09537104.2025.2547926","DOIUrl":"https://doi.org/10.1080/09537104.2025.2547926","url":null,"abstract":"","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2547926"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131771","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 testosterone on platelet activation and inflammation in transgender men.","authors":"Lieve Mees van Zijverden, Moya Henriëtte Schutte, Marieke Tebbens, Milou Cecilia Madsen, Jeske Joanna Katarina van Diemen, Chantal Maria Wiepjes, Martin den Heijer, Abel Thijs","doi":"10.1080/09537104.2025.2567294","DOIUrl":"https://doi.org/10.1080/09537104.2025.2567294","url":null,"abstract":"<p><strong>Background and aims: </strong>Transgender men (female sex assigned at birth, male gender identity) who use testosterone have a higher cardiovascular risk compared to women and men from the general population, which cannot be fully attributed to traditional cardiovascular risk factors. Platelet activation and (endothelial) inflammation are interconnected mechanisms in the process of primary hemostasis, and thus the development of cardiovascular disease, but the impact of testosterone on these mechanisms is largely unexplored. Hence, we aimed to investigate the effect of testosterone on platelet activation and inflammation in vivo.</p><p><strong>Methods: </strong>In this prospective cohort study 18 transgender men were included. Blood samples were taken at baseline and at 6, 12 and 52 weeks after testosterone initiation. We measured seven platelet activation markers (plasma thromboxane B2, Closure Time measured in two ways, CD63, CD62p, platelet-leukocyte complexes, immature platelet fraction), and twelve inflammation markers (high sensitivity CRP and 11 cytokines). Percentage changes relative to baseline were calculated at each time point using linear mixed model analyses.</p><p><strong>Results: </strong>Platelet activation markers CD63, CD62p, and platelet-leukocyte complexes exhibited an initial tendency to increase at week 6, then slightly decreased at week 12, and again increased at week 52. Closure Time and immature platelet fraction remained stable throughout the study period. The collective of inflammation markers exhibited an overall tendency toward increase throughout the study period, which was most pronounced at week 52.</p><p><strong>Conclusion: </strong>The results suggest that testosterone administration may increase platelet activation and inflammation. This may contribute to the higher cardiovascular risk in transgender men.</p><p><strong>Study registration: </strong>EudraCT #2017-003072-31.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2567294"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244878","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":"Cardiometabolic risk factor burden associates with an immature platelet profile.","authors":"Carine E Hamo, Matthew Muller, Emily Rosenfeld, Yuhe Xia, Adedoyin Akinlonu, Elliot Luttrell-Williams, Tessa J Barrett, Jeffrey S Berger","doi":"10.1080/09537104.2025.2459800","DOIUrl":"10.1080/09537104.2025.2459800","url":null,"abstract":"<p><p>Cardiometabolic risk factors, obesity, diabetes and hyperlipidemia contribute to cardiovascular disease (CVD). While platelets are involved in CVD pathogenesis, the relationship between risk factor burden on platelet indices and the platelet transcriptome remains uncertain. Blood was collected from CVD-free adults, measuring platelet count, mean platelet volume (MPV), immature platelet fraction (IPF), and absolute immature platelet fraction (AIPF) by hemogram. Platelets were isolated and analyzed via RNA sequencing. Participants were stratified by number of cardiometabolic risk factors (diabetes, obesity, hyperlipidemia). We calculated median (IQR) values of platelet indices and p-for-trend via linear regression across risk factor burden. To evaluate the association between risk factor burden and platelet transcripts, we performed multivariable linear regression adjusting for age, sex, and race/ethnicity. Among 141 participants, (50.5 ± 14.8 years, 42% male, 26% Black) risk factor burden was associated with increasing platelet size, IPF, and AIPF but not platelet count. Platelet RNA sequencing identified 100 differentially expressed transcripts (<i>p</i> < .01; 66 upregulated, 34 downregulated). Gene ontology enrichment analysis demonstrated upregulated pathways of secondary metabolic processes (NES = 1.96, <i>p</i> < .01), and hematopoietic stem cell proliferation (NES = 1.95, <i>p</i> < .01). Greater cardiometabolic risk factor burden is associated with increased platelet size and immaturity and suggesting novel platelet-mediated mechanisms linking risk factor burden with CVD.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2459800"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clopidogrel monotherapy is associated with higher mortality risk compared to aspirin: a retrospective analysis of NHANES 1999-2018.","authors":"Tieshi Zhu, Yong He, Yuzhang Bei, Hui Mai, Le Zhao","doi":"10.1080/09537104.2025.2532454","DOIUrl":"https://doi.org/10.1080/09537104.2025.2532454","url":null,"abstract":"<p><strong>Background: </strong>Clopidogrel and aspirin are widely used antiplatelet agents. Although clopidogrel resistance is more prevalent in Asian populations, a Korean study suggested that clopidogrel was superior to aspirin in patients who completed standard dual antiplatelet therapy following percutaneous coronary intervention. However, the comparative effectiveness of clopidogrel versus aspirin in populations with lower levels of clopidogrel resistance remains to be further investigated.</p><p><strong>Methods: </strong>This study included 1,007 participants from NHANES 1999-2018 who were receiving aspirin or clopidogrel monotherapy. Cox proportional hazards regression and Kaplan-Meier survival analyses were used to compare the risks of mortality between the two groups. Sensitivity analyses were conducted by excluding individuals who died within the first 6 months of follow-up.</p><p><strong>Results: </strong>Across all Cox models, clopidogrel use was associated with significantly higher risks of all-cause mortality (Model 1, HR1.47, 95%CI 1.20-1.79, <i>p</i> < .01; Model 2, HR1.25, 95%CI 1.02-1.54, <i>p</i> = .03; Model 3, HR 1.33, 95%CI 1.08-1.64, <i>p</i> = .01; Model 4, HR1.31, 95%CI 1.06-1.63, <i>p</i> = .01), stroke and cardiac mortality (Model 1, HR1.76, 95%CI 1.27-2.43, <i>p</i> < .01; Model 2, HR1.41, 95%CI 1.01-1.97, <i>p</i> = .04; Model 3, HR 1.54, 95%CI 1.10-2.17, <i>p</i> = .01; Model 4, HR1.47, 95%CI 1.03-2.08, <i>p</i> = .03) compared with aspirin. These associations remained consistent in sensitivity analyses. Kaplan-Meier survival curves also indicated higher risks of all-cause mortality, stroke and cardiac mortality in the clopidogrel group relative to the aspirin group.</p><p><strong>Conclusion: </strong>In this community-based population, clopidogrel monotherapy was associated with higher risks of all-cause mortality, stroke and cardiac mortality compared with aspirin.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2532454"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691325","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":"miR-28-5p targeted Rap1b attenuates splenic inflammation infiltration in immune thrombocytopenia.","authors":"Rongqing Yu, Lizhen Cen, Xinyu Wu, Huaiyuan Liu, Xuejun Zhai, Qiong Bin","doi":"10.1080/09537104.2025.2487756","DOIUrl":"10.1080/09537104.2025.2487756","url":null,"abstract":"<p><p>Immune thrombocytopenia (ITP) is an autoimmune disease with isolated platelet count decrease. A subset of patients responds inferiorly to the first-line therapies including glucocorticoid and intravenous immunoglobulins (IVIG), of which the underlying mechanisms have not been fully elucidated. We first found that expression of miR-28-5p was obviously increased in complete responders, and decreased to substantially low levels in partial or non-responders. In the passive ITP model, upregulation of miR-28-5p by injecting agomir slightly improved thrombocytopenia, and obviously inhibited the <i>Rap1b</i> gene expression. Luciferase reporter assay demonstrated there was significant decrease of luciferase activity in 293T cells co-transfected with miR-28-5p mimics and plasmids with <i>Rap1b</i> wide-type sequence. Upregulation of miR-28-5p, and downregulation of <i>Rap1b</i> played a favorable role in reducing B cell infiltration in the marginal zone of spleen in mice. However, miR-28-5p exhibited no significant influence on megakaryocyte maturation in ITP both in vitro and in vivo studies. Finally, we confirmed that miR-28-5p upregulation was associated with superior early treatment response in ITP, and possibly functioned by targeting <i>Rap1b</i> gene to inhibit humoral immunity.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2487756"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804089","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":"Complement C3 inhibition reduces complement activation in clinical platelet concentrates but does not counteract platelet storage lesions.","authors":"Linnea I Andersson, Per Sandgren, Dick J Sjöström, Camilla Mohlin, Kim Hägerström, Ivar Tjernberg, Tom Eirik Mollnes, Per H Nilsson","doi":"10.1080/09537104.2025.2513298","DOIUrl":"https://doi.org/10.1080/09537104.2025.2513298","url":null,"abstract":"<p><p>Platelet storage is associated with storage lesions, including platelet morphological changes and a gradual functional loss. We investigated the impact of complement C3 inhibition on complement activation and platelet storage lesions in clinical platelet concentrates. Platelet concentrates (<i>n</i> = 8) were prepared in PAS-E and stored for seven days at 22°C. Each concentrate was split in two, with the C3 inhibitor compstatin Cp40 added to one part, and the other serving as the control. Complement and platelet activation markers, platelet function, and metabolic measures were analyzed every second day. Cp40 significantly reduced C3bc and sC5b-9 levels, but not C4c, indicating inhibition of complement activation at the level of C3. However, Cp40 did not affect platelet-specific or metabolic measures. Surface expression of CD62P and NAP-2 release increased significantly over the storage time, whereas CD63 expression and PF4 and TSP-1 release remained stable. Platelet responses to TRAP-6 mediated PAR-1 activation and U46619 mediated TXA₂R stimulation decreased over time, recorded as CD62P and CD63 expression and release of soluble factors. No drop in platelet count was observed, and metabolic markers remained within their critical limits. While C3 inhibition effectively reduced complement activation in stored platelet concentrates, it did not mitigate platelet storage lesions.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2513298"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497794","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":"Differential effects of dual antiplatelet and dual antithrombotic therapy on hemostasis in chronic coronary syndrome patients: the DEFINE CCS study.","authors":"Tony Haddad, Osama Elkhateeb, Lawrence Title, Ata Quraishi, Wan Cheol Kim, Ali Hillani, Scott Grandy, Stefan S Heinze, Finn Eichhorn, Hannah Harquail, John Sapp, William Parker, Shamir R Mehta, Robert F Storey, Wael Sumaya","doi":"10.1080/09537104.2025.2524624","DOIUrl":"10.1080/09537104.2025.2524624","url":null,"abstract":"<p><p>Optimal long term antithrombotic treatment in high-risk chronic coronary syndrome (CCS) patients remains uncertain. Both ticagrelor (60 mg BID) and low-dose rivaroxaban (2.5 mg BID) in addition to low-dose aspirin resulted in significant reductions in major cardiovascular events in high-risk patients at the expense of increased bleeding risk. We aimed to compare the effects of both strategies on bleeding time, fibrin clot lysis time and inflammatory biomarkers in CCS patients with history of acute coronary syndrome. Twenty aspirin-treated patients were recruited into a randomized crossover study to receive ticagrelor 60 mg BID in 1 week and rivaroxaban 2.5 mg BID in the other with a 2-week washout period in between. Outcome measures were determined at the start and end of each treatment week. Two-way ANOVA was used to determine difference in treatment effect. Data are presented as mean ± SD. At baseline, there was no significant difference in any studied outcome measure. Bleeding time was significantly longer with ticagrelor compared to rivaroxaban (Ticagrelor: 897 ± 481secs vs. Rivaroxaban: 440 ± 184 secs; <i>p</i> = .0001). Fibrin clot lysis time was not impacted by ticagrelor but significantly dropped post treatment with rivaroxaban (Ticagrelor: 5743 ± 2590 secs vs. Rivaroxaban: 4309 ± 2308 secs; <i>p</i> = .0049). Neither treatment had an impact on levels of high-sensitivity CRP or white cell count. In conclusion, ticagrelor 60 mg BID has greater impact on bleeding time compared to rivaroxaban 2.5 mg BID. Whereas rivaroxaban, positively modulates fibrin clots, rendering them more prone to lysis.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2524624"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144554275","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":"Pharmacodynamic effects of early aspirin withdrawal after percutaneous coronary intervention in patients with atrial fibrillation treated with ticagrelor or prasugrel.","authors":"Mark A Sammut, Mohammed E F Rahman, Claire Bridge, Jessica Hanson, Heather Judge, Bethany Lynch, Emily Maz, Hannah McMellon, Janet Middle, Georgia Williamson, William A E Parker, Justin Lee, Robert F Storey","doi":"10.1080/09537104.2025.2507037","DOIUrl":"10.1080/09537104.2025.2507037","url":null,"abstract":"<p><p>Dual antithrombotic therapy (DAT) without aspirin reduces bleeding compared with triple antithrombotic therapy (TAT) in patients with atrial fibrillation who have undergone percutaneous coronary intervention, without apparently increasing ischemic events. A prospective pharmacodynamic study was performed to investigate the impact of aspirin on bleeding time, platelet function and fibrin clot analysis in this population. Patients receiving TAT (<i>n</i> = 16), comprising aspirin, ticagrelor/prasugrel and a direct-acting oral anticoagulant (DOAC), were compared with those receiving DAT without aspirin (<i>n</i> = 18). Bleeding time was reduced with DAT compared with TAT (median 27.8 vs 30.0 minutes, <i>p</i> = .005). Assessed by light transmission aggregometry, median platelet aggregation was significantly increased with DAT compared with TAT in response to arachidonic acid (63 vs 3%, <i>p</i> = .002) and collagen (72 vs 37%, <i>p</i> < .001) but not 5-μmol/L adenosine diphosphate (25 vs 27%, <i>p</i> = .966) or thrombin-receptor-activating peptide (37 vs 24%, <i>p</i> = .086). VerifyNow P2Y₁₂ assay showed > 70% inhibition in all patients. Fibrin clot lysis time and maximum turbidity were similar between groups. Using P2Y₁₂ inhibitors of consistent potency, DAT improves hemostasis through sparing cyclooxygenase-1-mediated platelet activation but has a comparable effect to TAT on other pathways and fibrin clot properties. DAT with ticagrelor/prasugrel and DOAC may provide sufficient antithrombotic effect without excessive anti-hemostatic effect.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2507037"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The NLRP3 inflammasome in platelets - form, functions, and future of the complex.","authors":"Matthew S Hindle, Martin Berger, Khalid M Naseem","doi":"10.1080/09537104.2025.2562267","DOIUrl":"https://doi.org/10.1080/09537104.2025.2562267","url":null,"abstract":"<p><p>Platelets are anucleate cells that primarily facilitate thrombosis and hemostasis but can also act as mediators of vascular inflammation in disease. Platelets are typically understood to do this through the release of pre-formed chemokines coupled with direct heterotypic interactions with a variety of immune cells. However, an alternative mode of action has been described where platelets are able to undertake <i>de novo</i> synthesis of the cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18). The primary mechanism to produce these inflammatory mediators is the activation of the NACHT leucine-rich repeat pyrin domain-containing protein 3 (NLRP3) inflammasome, a multi-protein complex that processes IL-1β and IL-18 through caspase activation. The presence and characteristics of the NLRP3 inflammasome have been widely described in a variety of nucleated cells, although its role in anucleate platelets is less clear. In the last decade, the presence of the inflammasome has been reported in platelets and linked to several diseased states including sickle cell disease, acute coronary syndrome, sepsis, and viral hemorrhagic fever. This emerging new biology of platelets, its role in platelet function, vascular inflammation, and other related areas of exploration are critically reviewed here.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2562267"},"PeriodicalIF":2.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131800","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":"CD39-Diannexin alleviates the platelet storage lesion by protecting platelets from activation, a new attempt from a traditional perspective.","authors":"Cheng Liu, Peng Wang, Yafei Gao, Xiaolong Ma, Yang Su, Yao Wei, Rui Qiao","doi":"10.1080/09537104.2025.2517108","DOIUrl":"https://doi.org/10.1080/09537104.2025.2517108","url":null,"abstract":"<p><p>Due to platelet storage lesions (PSL), transfused platelets are unable to function properly in the prevention and treatment of bleeding in critically ill patients. It is a traditional assumption that PSL is closely related to platelet activation during storage because of the exposure of CD62P, phosphatidylserine (PS), etc. In this standpoint, activated platelets in <i>vitro</i> cannot be reactivated in <i>vivo</i> to exert their hemostatic function and exposed PS accelerates platelet clearance. Therefore, reducing platelet activation is helpful to alleviate PSL. Diannexin is the dimer of annexin that has a higher affinity for PS. CD39 is an ADP hydrolase produced by the vascular endothelium. As a result, we construct CD39-Diannexin (CD39-DA) fusion protein and hypothesize that CD39-DA can reduce platelet activation during storage to alleviate PSL. CD39-DA can bind to the exposed PS on the surface of stored platelets by immunofluorescence. Compared to the control groups, CD39-DA reserves part of stored platelets' aggregation function confirmed by platelet aggregation assay, induced by AA, ADP and collagen. Additionally, CD39-DA reduces lactic dehydrogenase (LDH) levels and CD62P-positive events after three-day storage. Interestingly, we preliminarily discover that CD39-DA may reduce stored platelets' apoptosis and increase aggregatory platelets after activation by thrombin, collagen and calcium, which is marked by GSAO. In conclusion, we confirm that CD39-DA can alleviate PSL by reducing platelet activation.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2517108"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258820","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}