Platelets最新文献

{"title":"Developmental differences in platelet P-selectin expression modulate neonatal monocyte inflammatory responses.","authors":"Erin Soule-Albridge, Emily Flahardy, Henry A Feldman, Natalie Kane, Kimberley Banfield, Amalia El Nems, Jesselin Romero Escobar, Martha Sola-Visner, Patricia Davenport","doi":"10.1080/09537104.2026.2726287","DOIUrl":"10.1080/09537104.2026.2726287","url":null,"abstract":"<p><p>Neonatal and adult platelets are functionally different, with neonatal platelets being comparatively hypo-reactive to multiple platelet agonists. When transfused, neonates receive platelets from adult donors, resulting in a cellular developmental mismatch. Platelets are key regulators of the monocyte inflammatory response, yet how the developmental stage of the platelet affects this response is unknown. In this study, we modeled this developmental mismatch <i>in vitro</i> to investigate the neonatal (cord blood) monocyte inflammatory response and migratory phenotype after exposure to either neonatal (cord blood) or adult platelets. Adult platelets expressed more P-selectin on the surface and released more beta-2-microglobulin (B2M) after activation compared to neonatal platelets. While exposure to platelets of either developmental stage increased the release of IL-8 and MCP-1 from neonatal monocytes to a similar degree, exposure to adult platelets induced significantly greater monocyte CCR2 and CCR5 surface expression, consistent with a pro-migratory monocyte phenotype. Blocking P-selectin/PSGL-1 interactions had no effect on platelet induced monocyte cytokine release but completely abrogated monocyte CCR2 and CCR5 surface upregulation. These findings suggest that the monocyte pro-migratory phenotype is regulated by P-selectin exposure, which is influenced by the platelet developmental stage, while monocyte cytokine release is independent of platelet P-selectin expression or developmental stage.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2726287"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017746","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":"Autosomal dominant thrombocytopenia associated with the CYCS p.Arg92Gly variant: clinical characterization of an additional family and observation of antiplatelet tolerance.","authors":"Emad Muhammad, Eveline Shabbad, Alina Kurolap, Gharam Shama, Yarden Caspin, Sundus Gaban, Claudia Gonzaga-Jauregui, Amir Peleg, Hagit Baris Feldman, Meir Preis","doi":"10.1080/09537104.2026.2616296","DOIUrl":"10.1080/09537104.2026.2616296","url":null,"abstract":"<p><p>Thrombocytopenia 4 (THC4) is a rare autosomal dominant inherited thrombocytopenia caused by pathogenic variants in <i>CYCS</i>, the gene encoding cytochrome c. Although <i>CYCS</i>-related thrombocytopenia is well characterized as a mild, non-syndromic quantitative platelet disorder, few families have been described worldwide. Recently, the missense variant c.274A > G (p.Arg92Gly) was reported in a single family. Here, we describe an additional multi-generational family from the Middle East carrying the same variant, thereby providing independent confirmation of pathogenicity and expanding the available phenotypic data. Seven affected individuals exhibited stable, moderate thrombocytopenia (55-88 × 10⁹/L) with normal platelet size and morphology, normal platelet aggregation responses, and no syndromic features. One newborn presented with petechiae and grade 1 intracranial hemorrhage but recovered fully. Whole-exome sequencing identified p.Arg92Gly as the only variant segregating with disease; Sanger sequencing confirmed heterozygosity in all affected members. Structural modeling demonstrated loss of stabilizing hydrogen bonds involving a highly conserved residue within the C-terminal helical region of cytochrome c, likely impairing local structural stability. Importantly, one affected individual tolerated long-term aspirin and clopidogrel therapy following an ischemic stroke without bleeding complications-an observation not previously reported in THC4. This Brief Report strengthens the association between <i>CYCS</i> p.Arg92Gly and inherited thrombocytopenia and provides clinically important data regarding antiplatelet therapy safety in this rare condition.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2616296"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166280","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":"Durable platelet response and immature platelet indices following sequential efgartigimod and eltrombopag therapy in a patient with refractory ITP.","authors":"Fumiya Wada, Hiroyuki Matsui, Takuji Nakamura, Tomomi Satoh-Nakamura, Yutaka Shinkawa, Hisanori Umehara, Akifumi Takaori-Kondo","doi":"10.1080/09537104.2026.2710092","DOIUrl":"10.1080/09537104.2026.2710092","url":null,"abstract":"<p><p>Efgartigimod, a neonatal Fc receptor (FcRn) antagonist, represents a novel therapeutic approach for refractory immune thrombocytopenia (ITP). However, its clinical positioning and durability of response in real-world settings remain unclear. We describe a case of refractory ITP in which efgartigimod induced a partial response that was enhanced by the subsequent addition of a thrombopoietin receptor agonist (TPO-RA), resulting in durable remission after efgartigimod discontinuation. Subsequent hematologic workup revealed that platelet recovery was accompanied by a reciprocal shift in immature platelet indices, with immature platelet fraction percentage decreasing and absolute immature platelet fraction increasing. Although there is a paucity of literature on immature platelet indices during ITP treatment, these parameters may serve as useful biomarkers for monitoring therapeutic response. Notably, efgartigimod was discontinued after 22 weeks, with sustained response maintained for an additional 24 weeks on TPO-RA monotherapy. This treatment course highlights the potential of FcRn inhibition to induce durable immunomodulatory effects and demonstrates synergistic benefits with TPO-RAs-insights that extend beyond the scope of conventional clinical trial protocols.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":" ","pages":"2710092"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148606843","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 mitochondrial deacetylase SIRT3 is nonessential for cyclophilin D-dependent procoagulant platelet formation in mice.","authors":"Jens Van Bael, Anne-Sophie Delmote, Inge Pareyn, Laurence Pirotton, Emma de Cartier d'Yves, Sandrine Horman, Yotis A Senis, Johan Auwerx, Simon F De Meyer, Karen Vanhoorelbeke, Claudia Tersteeg","doi":"10.1080/09537104.2026.2721783","DOIUrl":"https://doi.org/10.1080/09537104.2026.2721783","url":null,"abstract":"<p><p>Sirtuin 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD)-dependent mitochondrial deacetylase that regulates protein acetylation and maintains mitochondrial homeostasis in nucleated cells. By deacetylating cyclophilin D (CypD), SIRT3 limits mitochondrial permeability transition pore (mPTP) opening and protects against mitochondrial dysfunction. Although SIRT3 is present in murine and human platelets, its contribution to platelet mitochondrial regulation and procoagulant platelet formation remains unknown. This study investigated whether platelet SIRT3 modulates CypD-dependent procoagulant platelet formation. Platelets obtained from platelet-specific Sirt3 knockout mice (<i>Sirt3</i>^{<i>plt-/-</i>}) and littermate controls (<i>Sirt3</i>^{<i>plt+/+</i>}) were analyzed under resting conditions and after activation with CRP-XL and thrombin. Flow cytometry was used to analyze platelet (activation) markers and procoagulant platelet formation, and mitochondrial respiration was assessed using a Seahorse extracellular flux analyzer. Platelets lacking SIRT3 showed no alterations in basal or agonist-stimulated mitochondrial respiration. Likewise, platelet <i>Sirt3</i> deletion did not affect the generation of procoagulant platelets in response to strong dual agonist stimulation. These findings indicate that, despite its role in regulating mPTP opening in nucleated cells, platelet SIRT3 is not required for procoagulant platelet formation, suggesting that platelets rely on distinct mechanisms for mPTP regulation.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2721783"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888030","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":"Sex differences in fecal microbiota transplantation for mitigating radiation-induced thrombocytopenia in mice: efficacy amplified by inulin.","authors":"Qian Jia, Huan Wang, Wen Yin, Chao Zhang, Xinxin Xu, Sicheng Liang, Wen Pan, Bo Tang, Wanmeng Xiao, Sha Liu, Muhan Lü","doi":"10.1080/09537104.2026.2701022","DOIUrl":"10.1080/09537104.2026.2701022","url":null,"abstract":"<p><strong>Background: </strong>Fecal microbiota transplantation (FMT) shows potential in promoting hematopoiesis, with efficacy influenced by donor sex. However, its role in radiation-induced thrombocytopenia (RIT) and its sex-specific effects remain unclear. While inulin may enhance FMT efficacy, this has not been explored in the context of RIT.</p><p><strong>Methods: </strong>We established an irradiation-induced thrombocytopenia (RIT) model in male and female mice via 4 Gy X-rays exposure. FMT was administered orally as a fecal suspension. Platelet recovery was monitored via hematology analyzer, megakaryopoiesis was assessed by flow cytometry and H&E staining; gut microbiota changes were evaluated by 16S rRNA sequencing.</p><p><strong>Results: </strong>Sex-matched FMT accelerated platelet recovery and promoted megakaryocyte production in the bone marrow and spleen only in female mice, accompanied by an increase in <i>Akkermansia</i> abundance. Furthermore, transplanting feces from female donors also accelerated platelet recovery in irradiated male mice, whereas feces from male donors does not. INU selectively enriched probiotic colonization, thereby fostering a favorable microbial structure that enhanced FMT efficacy.</p><p><strong>Conclusions: </strong>The sexually dimorphic gut microbiota contributes to sex-specific FMT efficacy in alleviating radiation-induced thrombocytopenia, which can be further amplified by inulin. This study offers sex-specific microbial therapy for radiation-induced thrombocytopenia and a prebiotic-based strategy to boost FMT efficacy.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":" ","pages":"2701022"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670428","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":"Insomnia is associated with altered arachidonic acid-induced platelet aggregation and lower cholesterol independent of age in aspirin-treated unstable angina: a machine learning analysis.","authors":"Jirao Shen, Yiming Ma, Liyun Zheng, Yajie Wang, Xinran Liu, Yuan Zhang, Xiaofei Li","doi":"10.1080/09537104.2026.2743142","DOIUrl":"https://doi.org/10.1080/09537104.2026.2743142","url":null,"abstract":"<p><strong>Background: </strong>In aspirin-treated unstable angina (UA), heterogeneity in on-treatment arachidonic acid (AA)-induced platelet aggregation and cholesterol reduction contributes to residual ischemic risk. Insomnia is prevalent in coronary disease, yet its association with specific aspirin-sensitive platelet aggregation kinetics and lipid parameters remains undefined.</p><p><strong>Methods: </strong>In a cross-sectional cohort of 198 aspirin-treated UA patients, 38 routine hematologic or biochemical variables including AA-induced platelet aggregation indices were analyzed using principal component analysis (PCA) and unsupervised phenotyping (k-means and hierarchical clustering). Elastic-net logistic regression and machine learning classifiers were used for multivariable modeling, and performance was estimated by cross-validation. Correlation-network analysis and Shapley additive explanations (SHAP) supported interpretability.</p><p><strong>Results: </strong>Unsupervised analyses consistently identified two phenotypes. Insomnia was enriched in a platelet-lipid phenotype characterized by lower platelet aggregation indices and a lower lipid marker profile. The K-nearest neighbors (KNN) model demonstrated strong cross-validated discrimination (AUC = 0.934; average precision = 0.923), while all four classifiers converged with AUC > 0.925. After age matching, elastic-net logistic regression retained only AA-induced maximal platelet aggregation (PmaxAggR) and total cholesterol (CHOL) as independent predictors, with odds ratios of 0.927 and 0.340, respectively (both <i>p</i> < .001). Inflammatory markers, including neutrophil count and monocyte count, were no longer selected. Network analysis placed insomnia within the platelet-lipid module linked to PMaxAggR, CHOL, and some other platelet or lipid indices.</p><p><strong>Conclusions: </strong>In age-matched, aspirin-treated UA patients, insomnia is independently associated with reduced PMaxAggR and lower CHOL, with inflammatory markers no longer significant after age-balancing. These findings delineate an age-independent platelet-cholesterol axis linked to insomnia, potentially reflecting shared autonomic and neurobiological dysregulation, and motivate sleep evaluation as part of platelet-reactivity phenotyping in this population.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2743142"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128633","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":"Glycocalicin is contained inside the thrombus.","authors":"Caitlin Debaene, Katrijn R Six, Sarah Vertongen, Carine De Buck, Hendrik B Feys","doi":"10.1080/09537104.2026.2743143","DOIUrl":"https://doi.org/10.1080/09537104.2026.2743143","url":null,"abstract":"<p><p>Glycoprotein Ibα (GPIbα) is a platelet-specific receptor that is subjected to proteolytic shedding by ADAM17, releasing its ectodomain glycocalicin. GPIbα proteolysis is induced by strong platelet activation in a process too slow to be crucial in primary hemostasis. The spatiotemporal fate of glycocalicin was assessed during thrombosis using human and murine samples, integrating <i>in vitro</i> approaches and an inferior vena cava (IVC) ligation model. We found that the glycocalicin concentration inside human thrombi was 4-fold higher than in initial plasma (4.0 ± 0.8 µg/mL vs 0.9 ± 0.0 µg/mL, respectively). This was confirmed <i>in vitro</i> starting from human platelet-rich plasma or murine whole blood, with 6-fold and 3-fold increases, respectively. <i>In vivo</i>, containment of glycocalicin inside thrombi following IVC ligation was even more pronounced with glycocalicin levels reaching 135.1 ± 44.3 µg/mL in thrombi compared to 8.2 ± 1.0 µg/mL in plasma. In the presence of ADAM17 inhibitors, the glycocalicin concentration inside human thrombi was 3-fold lower than in thrombi with competent ADAM17. In contrast, inhibition of ADAM17 in mice, either pharmacologically or genetically, had no limiting effect on intrathrombic GPIbα shedding. In conclusion, GPIbα shedding occurs inside thrombi and results in maximal retention of glycocalicin. Intrathrombic GPIbα shedding is conserved between species, but is regulated differently.<b>KEY POINTS</b> Glycocalicin is contained within the thrombus microenvironmentRegulation of GPIbα ectodomain shedding is species-dependent and not universally mediated by ADAM17.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2743143"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195794","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":"A new mouse model of thrombopoietin deficiency arising from a spontaneous single base pair mutation.","authors":"Nan Sophia Han, Emma E Yvanovich, Shenglin Mei, Harvey G Roweth, Elisabeth M Battinelli, David B Sykes, Ninib Baryawno","doi":"10.1080/09537104.2025.2602721","DOIUrl":"https://doi.org/10.1080/09537104.2025.2602721","url":null,"abstract":"<p><p>Thrombopoietin (TPO) is the principal regulator of bone marrow platelet production and plays an important role in maintaining hematopoietic stem and progenitor cells. Predominantly produced in the liver, circulating TPO levels are primarily modulated through receptor-mediated clearance of TPO by target cells such as platelets. However, there is an additional component of TPO regulation at the transcriptional level, which may be affected in the setting of platelet-associated diseases. Current TPO knockout mouse models partially limit the study of transcriptional regulation because of disruption of the TPO genomic locus. Here, we describe a novel mouse model of TPO deficiency arising from a spontaneous mutation in a single base pair within exon 5 of the TPO gene. The resulting amino acid change (leucine to histidine at position 121) predicts a dramatic alteration in protein structure, ultimately resulting in a ~ 95% decrease of circulating TPO. The hematological phenotype of this new <i>C57Bl/6(IMPC)J-TPO</i>^<i>L121H</i> strain mimics that of other mouse models of TPO deficiency, but the genomic locus remains intact and therefore preserves normal TPO transcriptional regulation. We characterize the hematological phenotype of this new strain and discuss its applications as a model of transcriptional TPO regulation and clinical thrombocytopenia. Our findings highlight the theoretical possibility that TPO protein destabilizing mutations may explain rare cases of patient thrombocytopenia.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2602721"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850690","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":"Assessing mitochondrial function and protein composition in platelet-derived extracellular vesicles.","authors":"Vanessa Veilleux, Nicolas Pichaud, Gilles A Robichaud, Luc H Boudreau","doi":"10.1080/09537104.2025.2610264","DOIUrl":"https://doi.org/10.1080/09537104.2025.2610264","url":null,"abstract":"<p><p>Platelets, traditionally known for their role in hemostasis, also contribute to inflammation, cancer, and intercellular communication through the release of platelet-derived extracellular vesicles (or platelet-derived microparticles; PMPs). Among these vesicles, a subpopulation containing functional mitochondria, known as mitoMPs, can be transferred to recipient cells, thereby modulating their metabolism and biological responses. This mitochondrial transfer plays a key role in various pathological processes, where it may either restore metabolic functions or enhance cancer cell proliferation, survival, and metabolic plasticity. In this study, we developed a permeabilization protocol combined with high-resolution respirometry to assess mitochondrial respiration in both platelets and PMPs. First, we found that saponin was a more effective permeabilizing agent than digitonin to measure mitochondrial respiration in these models. Moreover, our analysis revealed distinct respiratory profiles between platelets and PMPs and demonstrated that freeze-thaw cycles severely compromise mitochondrial functions in PMPs. Additionally, we performed proteomic profiling of PMPs to characterize their protein cargo, which associate with specific molecular pathways, particularly those associated with mitochondrial metabolism. These results provide novel insights into the biological functions of PMPs and their potential involvement in disease processes. Together, these findings advance the understanding of PMP-mediated mitochondrial transfer and intercellular communication and establish a foundation for future biomedical and therapeutic investigations.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2610264"},"PeriodicalIF":2.6,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145900498","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":"Oleanolic acid, a herb extract, acts as a strong and safe enhancer in the collagen-mediated hemostatic cascade in flow.","authors":"Dailin Chen, Shaopeng Xu, Xuqiang Gao, Ying Yang, Harsh M Trivedi, Jinhui Ma, Yichong Luo, Jianfang Ren, Yong Chen, Jianhua Wu, Ying Fang","doi":"10.1080/09537104.2026.2703628","DOIUrl":"https://doi.org/10.1080/09537104.2026.2703628","url":null,"abstract":"<p><p>Considerable attention has been paid steadily for efficacy and safety of herb extracts with medicinal benefits, recently. Tranexamic acid (TXA) is a well-known hemostatic agent with strong efficacy but potential thrombus risk. Here, we identified oleanolic acid (OA) as a strong enhancer in promoting adhesion, spreading or aggregation of platelets on immobilized collagen, which exceeds TXA among six herb extracts. In addition, the study demonstrated that TXA could facilitate morphological changes of platelets on collagen, accelerate and enhance intracellular calcium bursting with and without mechanical stimulus, which might cause an excessive hemostatic response and lead to thrombus. While OA exerted a comparable effect specifically under low-shear flow regimes, providing a flow-assisted chemical activation that bypasses the need for high-magnitude mechanical tension but ensures localized efficacy. In summary, this study identified OA as a herbal coagulant that showed hemostatic efficacy similar to TXA, but with a better safety profile. It provided a new insight into the flow-assisted mechanism underlying hemostatic efficiency and should be useful in finding novel and safe hemostatic drugs and in developing a practical method for functional identification of hemostatic agents.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"37 1","pages":"2703628"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875831","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}