BLOOD血液
BLOOD(英文缩写 BLOOD),ISSN 0006-4971,eISSN 1528-0020,中文译名:血液 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 25.669 | Q1 |
| 2022 | 20.300 | Q1 |
| 2023 | 21.000 | Q1 |
| 2024 | 23.100 | Q1 |
| 2025 | 23.900 | Q1 |
BLOOD 最新收录文献
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1. DMT1 Facilitates Heme-iron Absorption in Rats and Mice.
1. DMT1促进大鼠和小鼠的血红素铁吸收PMID:日期:2026-10-02Mechanisms of heme-iron (HI) absorption remain uncertain. Heme is probably absorbed by receptor-mediated endocytosis; iron is then enzymatically liberated from heme within endosomes, or in the cytosol. If heme is catabolized in endosomes, a transporter, such as DMT1, would be required to export ionic iron into the cytosol. Here, we tested the hypothesis that intestinal DMT1 functions in the HI absorption pathway. The first experimental approach utilized Belgrade (b) rats, expressing dysfunctional DMT1 protein, and the second used conditional, intestine-specific DMT1 KO mice. HI absorption experiments were carried out with radiolabeled, donor rat RBCs, containing ~98% of iron as HI and with >94% of activity in 59Fe-heme. Iron-deficient, anemic +/b (control) rats absorbed 10.8% of a peroral dose of 59Fe-heme within 24 hours, while similarly anemic b/b rats absorbed 1.4% (an 8-fold reduction). Notably, serum hepcidin levels were invariable between both groups of rats (and 10x lower than controls). Moreover, ablation of intestinal DMT1 led to iron-restricted erythropoiesis and severe anemia in adolescent mice weaned on to nonheme iron (NHI) or HI diets. DMT1 was also required to upregulate 59Fe-heme absorption in iron-deficient, anemic mice. DMT1 thus facilitates the absorption of both main forms of dietary iron, NHI and HI.
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2. New FDA-Approved Treg Therapy to Reduce Chronic GVHD After Allogeneic HSCT.
2. FDA新批准的Treg疗法用于减少异基因HSCT后慢性GVHDPMID:日期:2026-10-02The Precision-T phase 3 trial is the first randomized, multicenter demonstration that a centrally manufactured defined allograft is effective markedly reducing moderate-to-severe chronic GVHD and non-relapse mortality without loss of graft versus leukemia or graft failure and infection. The engineered graft appears to instruct immune reconstitution toward a regulated, tolerance-associated state, giving the product a mechanism for further studies. The question is how far we can further program it.
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3. Enhanced factor VIII activation accelerates thrombin generation and hemostatic potency in mice.
3. 增强的因子VIII激活加速小鼠体内凝血酶生成和止血效能PMID:日期:2026-10-01Factor VIII (FVIII) circulates as an inactive procofactor and is converted to its active form (FVIIIa) by proteolytic cleavage at Arg372, Arg740, and Arg1689. Although these cleavage events are well characterized, their individual contributions to FVIII activation and hemostatic function remain incompletely defined. To address this, we engineered a FVIII variant (FVIII-2RKR) in which the B-domain and acidic region 3 region were replaced with a PACE/furin processing site, generating a molecule that requires only cleavage at Arg372 for conversion to FVIIIa. FVIII-2RKR exhibited markedly increased apparent activity in plasma-based assays, shortened thrombin generation lag time, and enhanced factor Xa (FXa) generation compared with B-domain-deleted FVIII, whereas both proteins were functionally equivalent following thrombin activation. FVIII-2RKR was cleaved more rapidly at Arg372 by thrombin and FXa, demonstrating that processing at Arg740 and Arg1689 regulates the rate of Arg372 cleavage rather than directly contributing to cofactor activity. In hemophilia A mice, FVIII-2RKR consistently enhanced early hemostatic function across ferric chloride, laser injury, and tail bleeding models, achieving improved efficacy at lower doses. Despite reduced half-life due to impaired von Willebrand factor (vWF) binding, FVIII-2RKR remained effective in vWF-deficient mice, indicating that vWF is not required for local FVIII function at sites of vascular injury. Together, these findings define distinct roles for FVIII activation cleavage sites and demonstrate that processing at Arg740 and Arg1689 regulates activation through Arg372, linking the rate of FVIII activation to hemostatic efficacy in vivo.
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4. --Paneth cell niche function is critical for intestinal stem cells in radiation injury but dispensable in GVHD.
4. --潘氏细胞微环境功能在放射性损伤中对肠道干细胞至关重要，但在移植物抗宿主病中并非必需PMID:日期:2026-10-01Paneth cells (PCs) produce WNT3 and EGF in the small intestine and are thought to contribute to the intestinal stem cell (ISC) niche, which is a target of graft vs. host disease (GVHD). However, PC deletion models have failed to demonstrate substantial consequences for ISCs or other epithelial pathology. The physiologic role of PC niche function has thus remained opaque, and the significance of this function after bone marrow transplantation (BMT) is poorly understood. Using Lysozyme1-DTR mice to ablate PCs, we found stable WNT3 expression in vivo, and crypts from PC-ablated mice retained organoid-forming capacity, further reflecting persistent WNT3 production. However, PC ablation reduced EGF expression and increased intestinal radiation injury. Irradiated PC-deficient mice exhibited attenuated epithelial regeneration and exacerbated ISC and crypt loss, which were restored by exogenous EGF administration, thus indicating EGF-dependent PC contributions in radiation injury. In contrast, after allogeneic BMT, PC ablation and the associated EGF reduction had no substantial impact on intestinal pathology or systemic GVHD. WNT3 levels were comparable between PC-intact and PC-deficient BMT recipients, and other secretory cells emerged as potential alternative WNT3 sources. Furthermore, human duodenal biopsies from transplant patients demonstrated persistence of goblet and enteroendocrine cells in clinical GVHD, despite PC reductions, resulting in overall stable secretory lineage frequencies. These findings highlight an essential role for PC niche function as a nonredundant source of EGF in radiation injury. However, this function is dispensable in experimental GVHD. PC reductions in GVHD may thus reflect injury severity more than they contribute to it.
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5. Inhibition of mitochondrial permeability transition selectively suppresses thrombogenic platelet procoagulant activity.
5. 抑制线粒体通透性转换可选择性地抑制促血栓形成的血小板促凝血活性PMID:日期:2026-10-01Platelets support coagulation by externalizing phosphatidylserine (PS), creating a catalytic surface for thrombin generation and fibrin formation. Although platelet PS exposure is required for hemostasis, excessive procoagulant platelet activity drives thrombosis. Sustained calcium influx after strong agonist stimulation promotes mitochondrial permeability transition pore (mPTP) opening, mitochondrial depolarization and calcium amplification that commit platelets to PS-high procoagulant states. Existing approaches to suppress this pathway are limited by the hemostatic requirement for platelet PS exposure and pleiotropic effects of cyclophilin-targeting agents. Here, we use a series of newly developed cyclophilin D-independent small molecule mPTP inhibitors to define how mPTP opening regulates procoagulant platelet activity. Under GPVI/PAR-driven procoagulant conditions, MC63, TR001 and TR002 preserved mitochondrial membrane potential, prevented intracellular calcium overload and reduced PS/P-selectin-positive platelets, microparticle release and membrane blebbing, while preserving agonist-induced calcium mobilization, secretion, integrin activation, aggregation, F-actin assembly and clot retraction. Mechanistically, mPTP inhibition limited calcium-dependent phosphatase, protease and mitochondrial activities associated with procoagulant platelet conversion. MC63, TR001 and TR002 reduced platelet-dependent thrombin generation and fibrin formation without affecting platelet-independent thrombin activity. In whole blood perfused over collagen, mPTP inhibitors reduced PS-positive platelets within thrombi without impairing platelet accumulation. In vivo, mPTP inhibitors decreased platelet and fibrin accumulation after laser-induced arteriolar injury but did not prolong tail bleeding alone or in combination with acetylsalicylic acid. Together, these findings identify mPTP opening as a druggable checkpoint for platelet procoagulant commitment and support mPTP inhibition as an antithrombotic strategy that may preserve hemostasis.
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6. Fetal Anemia and Hemodynamic Adaptation in Hemoglobin H Disease: A Longitudinal Prospective Study.
6. 血红蛋白H病中的胎儿贫血与血流动力学适应：一项纵向前瞻性研究PMID:日期:2026-10-01Hemoglobin H (Hb H) disease, including deletional (Hb H-del) and non-deletional forms such as Hb H-Constant Spring disease (Hb H-CS), is highly prevalent in Asia. Its natural history and fetal hemodynamic changes remain inadequately characterized. The objective of this study is to characterize the natural history of fetal anemia and associated hemodynamic alterations in Hb H-del and Hb H-CS. At-risk pregnancies identified through α-thalassemia carrier screening prospectively underwent serial assessment of fetal anemia using middle cerebral artery-peak systolic velocity (MCA-PSV) and hemodynamic parameters using fetal echocardiography. Cordocentesis and intrauterine transfusion (IUT) were performed when indicated. Neonatal hematologic and genotypic evaluations were conducted postnatally. Among 389 at-risk pregnancies, 60 fetuses had Hb H-del and 22 had Hb H-CS. MCA-PSV MoM was significantly elevated in affected fetuses, particularly in Hb H-CS. In affected fetuses, MCA-PSV increased after mid-gestation, reached the highest level in the late second to early third trimester, and partially normalized near term. Cardiac enlargement, Tei index, and cardiac output were significantly increased, more prominently in Hb H-CS. Rates of significant anemia, reflected by MCA-PSV>1.5 MoM, and hydrops were higher in Hb H-CS than Hb H-del; 22.7% vs 13.6% and 8.3% vs 1.7%, respectively. In conclusion, Hb H disease is characterized by an exacerbation of fetal anemia and cardiac overload after mid-gestation with more severity in Hb H-CS fetuses. These findings provide a rationale for incorporating antenatal assessment into the management of pregnancies affected by Hb H disease and support further evaluation of proactive intrauterine management strategies in selected cases.
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7. Leukemia-associated myeloid cells support distinct T-ALL subtypes via unique signals converging on metabolic alterations.
7. 白血病相关髓系细胞通过汇聚于代谢改变的独特信号，支持不同的T-ALL亚型PMID:日期:2026-10-01Although intensified chemotherapy regimens have improved survival of T-cell acute lymphoblastic leukemia (T-ALL) patients, treatment-related toxicities and poor outcomes following relapse highlight the need for alternative therapeutics. Our previous studies showed that leukemia-associated myeloid cells support T-ALL progression, suggesting myeloid cells or associated signals could serve as therapeutic targets. It remains unknown whether leukemia-associated myeloid cells support multiple molecular subtypes of T-ALL, and if so, whether subtype-specific mechanisms are involved. We demonstrate that tumor-associated myeloid cells support survival of both Early T-cell Progenitor (ETP)-like and non-ETP-like T-ALL subtypes from the LMO2 mouse model in vitro and in vivo. Transcriptional profiling and in vitro assays of mouse and human T-ALL reveal that myeloid cells support distinct T-ALL subtypes via different signaling pathways: IL6ST/STAT3 signaling supports ETP-like T-ALL, while growth factor receptor signaling supports non-ETP-like T-ALL. Notably, both subtypes require AKT activation for myeloid-mediated support, and acute myeloid depletion in vivo induces a common metabolic shift towards oxidative phosphorylation (OxPhos). These findings suggest that myeloid cells promote T-ALL survival via subtype-specific signals that converge on a common pathway regulating metabolism. The shared metabolic adaptation to myeloid cell loss suggests a compensatory mechanism enabling T-ALL persistence under stress. Consistent with this possibility, combining myeloid depletion with OxPhos inhibition reduces survival of mouse and patient T-ALL cells and prolongs leukemic mouse survival more than either single treatment. Our data highlight unique and shared mechanisms by which myeloid cells support T-ALL subtypes and implicate tumor-myeloid interactions and downstream metabolic reprogramming as promising therapeutic targets.
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8. Functional Classification of Monoallelic TP53 Mutations Refines Prognostic Stratification in Myelodysplastic Neoplasms.
8. 单等位基因TP53突变的功能分类优化了骨髓增生异常肿瘤的预后分层PMID:日期:2026-10-01TP53 mutations represent one of the strongest adverse prognostic factors in myelodysplastic neoplasms (MDS). While multi-hit TP53 (TP53multiHit) alterations uniformly lead to very poor outcomes, the prognostic relevance of monoallelic TP53 (TP53mono) mutations remains controversial. TP53 variants can cause dominant-negative, loss-of-function, or gain-of-function effects. We hypothesized that functional heterogeneity among TP53 variants contributes to the variable clinical behavior observed in TP53mono-mutated MDS. Therefore, we analyzed pretreatment samples from 4,505 patients with MDS from two independent cohorts (IWG: n=3,173; J-MDS: n=1,332), including 271 patients with TP53mono and 499 with TP53multiHit. Functional annotation of TP53 variants was performed using a previously published phenotype score (PS) derived from saturation mutagenesis screens, capturing dominant-negative and loss-of-function effects. Median leukemia-free survival (LFS) differed significantly by TP53 allelic state (TP53 wild-type (TP53wt) 37.2 months; TP53mono 19.2 months; TP53multiHit 7.8 months; p<0.001). Within the TP53mono subgroup, functional annotation identified marked heterogeneity. Patients with high PS (≥7) showed a significantly inferior median LFS compared with those with low PS (12.6 vs. 43.3 months; p<0.001), particularly for IPSS-R and IPSS-M low-risk cases. Combining PS and variant allele frequency (VAF) further improved risk stratification. TP53mono patients with PS ≥7 and VAF ≥22% had a median LFS comparable to TP53multiHit cases (9.2 vs. 7.8 months, p=0.3), whereas those with PS <7 and VAF <22% exhibited a median LFS similar to TP53wt cases (44.7 vs. 37.2 months, p=0.8). Overall, functional annotation of TP53 variants refines prognostication in TP53mono-mutated MDS and may enhance individualized risk assessment.
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9. Mevalonate Metabolism Orchestrates Platelet Hyperactivation via Protein Prenylation to Aggravate Septic Thrombosis.
9. 甲羟戊酸代谢通过蛋白异戊烯化调控血小板过度活化从而加重脓毒症血栓形成PMID:日期:2026-10-01Sepsis is a life-threatening systemic inflammatory disorder that triggers disseminated intravascular coagulation and microthrombosis, in which exaggerated platelet activation exacerbates disease progression. The mevalonate pathway is responsible for the biosynthesis of vital isoprenoids and sterols, also playing an important role in the prenylation modification of proteins. We found the mevalonate metabolic pathway is highly activated in platelets during infection. The interruption of this pathway, using platelet specific mevalonate kinase deficiency mice model, could significantly suppress platelet activation and NETosis, alleviating sepsis-induced intravascular thrombosis. Mechanistically, we identified prenylated proteins in platelets and found prenylation level of small GTPases, such as Rap1, were increased after sepsis, indicating the important role of protein prenylation in platelet hyperactivation during sepsis. Notably, the binding level of Rap1 and Talin-1 was significantly impaired in MVK deficient platelets, showing that Rap1-Talin-1 interaction is crucial for MVA-mediated platelet activation. Furthermore, as inhibitors of prenyl diphosphate synthase, the lipophilic bisphosphonates TH-Z145 and TH-Z93 exerted potent effects in alleviating platelet activation and septic thrombosis, as well as prolonging survival in sepsis mice. Collectively, targeting the MVA pathway provides a novel therapeutic strategy for sepsis-triggered thrombosis and platelet activation.
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10. Efficacy and safety of tirabrutinib monotherapy for relapsed/refractory primary CNS lymphoma: PROSPECT phase 2 trial.
10. 替拉布鲁替尼单药治疗复发/难治性原发性中枢神经系统淋巴瘤的疗效和安全性：PROSPECT 2期试验PMID:日期:2026-10-01Primary central nervous system lymphoma (PCNSL) is an aggressive subtype of non-Hodgkin lymphoma with a poor prognosis, high rate of refractory or relapsed (R/R) disease, and no established standard of care for R/R PCNSL. This phase 2 study evaluated the efficacy and safety of tirabrutinib, a potent, highly selective, second-generation Bruton tyrosine kinase inhibitor, in patients with R/R PCNSL in the US. In the open-label PROSPECT study, adults with R/R PCNSL whose disease progressed on or after ≥1 high-dose methotrexate-based therapy received once-daily oral tirabrutinib 480 mg. The primary endpoint was overall response rate (ORR), and secondary endpoints included complete response (CR) rate, duration of response (DOR), and time to response (TTR), as assessed by independent review committee. Safety was assessed by frequency and severity of treatment-emergent adverse events (TEAEs). Among 48 enrolled patients, median follow-up was 11.5 months, ORR was 67% (95% confidence interval [CI], 52-80), and CR rate was 44% (95% CI, 29-59). Median DOR was 9.3 months (95% CI, 4.6-14.6), and median TTR was 1.0 month (range, 0.9-3.7). Treatment-related TEAEs occurred in 36 patients (75%), most commonly anemia (19%), maculopapular rash (17%), fatigue (15%), neutropenia (15%), lymphocytopenia (15%), pruritus (15%), and other rash (15%). Grade ≥3 treatment-related TEAEs occurred in 13 patients (27%), most commonly neutropenia (8%) and maculopapular rash (6%). One death (bronchopulmonary aspergillosis) was treatment related. In patients with R/R PCNSL, once-daily oral tirabrutinib monotherapy resulted in rapid and durable responses and demonstrated a favorable safety profile. This trial was registered at www.clinicaltrials.gov as NCT04947319.