Current Opinion in Hematology最新文献

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Advances in the pathophysiology and treatment of anaemia in multiple myeloma. 多发性骨髓瘤贫血的病理生理及治疗进展。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-11 DOI: 10.1097/MOH.0000000000000911
Nicola Giuliani, Benedetta Dalla Palma, Laura Notarfranchi
{"title":"Advances in the pathophysiology and treatment of anaemia in multiple myeloma.","authors":"Nicola Giuliani, Benedetta Dalla Palma, Laura Notarfranchi","doi":"10.1097/MOH.0000000000000911","DOIUrl":"10.1097/MOH.0000000000000911","url":null,"abstract":"<p><strong>Purpose of review: </strong>Anaemia is a common sign in multiple myeloma due to multifactorial mechanisms. Apart from the well known factors related to the disease, more recently, the use of several new drugs as the immunotherapeutic ones indicates the emerging role of drug-related mechanisms in the pathophysiology of anaemia in multiple myeloma patients.</p><p><strong>Recent findings: </strong>Anaemia associated with immunomodulatory drugs may result from both direct effect on hematopoietic progenitor cells and indirect one mediated by cytokine modulation within the bone marrow microenvironment. The CD38 expression by erythroid lineage cells, suggests that anti-CD38 antibodies may induce apoptosis or functional inhibition of these progenitors, leading to reductions in erythropoiesis. Recent clinical trials also reported ad high incidence of anaemia in multiple myeloma patients treated either with bispecific antibodies or CAR-T cells.Treatment of anaemia in multiple myeloma patients included the use of red blood cell transfusion and erythropoietin-stimulating agents but recently novel agents were under investigation as the activin receptor fusion proteins.</p><p><strong>Summary: </strong>The use of the new immunotherapeutic drugs in multiple myeloma patients is associated with an increased incidence of anaemia that should be considered by clinicians particularly in the management of those patients in which coexist other anaemia-related factors.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"65-72"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168127","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}
引用次数: 0
Protease-activated receptors in endothelial health and dysfunction. 蛋白酶激活受体在内皮健康和功能障碍中的作用。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-18 DOI: 10.1097/MOH.0000000000000915
Kaushik Muralidharan, Livia M Bogdan, Bryce A Kerlin
{"title":"Protease-activated receptors in endothelial health and dysfunction.","authors":"Kaushik Muralidharan, Livia M Bogdan, Bryce A Kerlin","doi":"10.1097/MOH.0000000000000915","DOIUrl":"10.1097/MOH.0000000000000915","url":null,"abstract":"<p><strong>Purpose of review: </strong>Protease-activated receptors (PARs) connect extracellular proteolytic activity to intracellular signaling in endothelial cells, placing them at the crossroads of coagulation, inflammation, and vascular stability. This review highlights recent progress in understanding endothelial PAR1-PAR4 signaling, focusing on how protease specificity, receptor interactions, and signaling bias shape endothelial responses in both health and disease.</p><p><strong>Recent findings: </strong>New research shows that endothelial PAR signaling varies greatly depending on the context. PAR1 displays biased signaling based on the type of protease and cleavage site, with thrombin mainly causing barrier disruption, while activated protein C (aPC) promotes cytoprotection via β-arrestin pathways. PAR2 processes signals from coagulation and inflammatory proteases to control endothelial inflammation, vasodilation, and paracrine signaling. Once considered a passive cofactor, PAR3 is now seen as an active regulator that forms heterodimers with PAR1, allowing engineered bivalent agonists to mimic protective aPC signaling. Notably, PAR4, a low-abundance but potent endothelial receptor, activates under conditions rich in proteases, leading to cytoskeletal changes, barrier dysfunction, and thromboinflammation.</p><p><strong>Summary: </strong>These insights reposition endothelial PARs as sophisticated sensors of the vascular protease environment. Future therapies are moving away from broad receptor blocking toward pathway-specific modulation that maintains protective signaling while reducing vascular damage, opening new avenues for precise vascular treatments.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"81-87"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328268","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}
引用次数: 0
The interface of hemostasis and inflammation: endothelial-platelet dynamics in thrombosis. 止血与炎症的界面:血栓形成中的内皮-血小板动力学。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-03-10 DOI: 10.1097/MOH.0000000000000918
Siobhan Branfield
{"title":"The interface of hemostasis and inflammation: endothelial-platelet dynamics in thrombosis.","authors":"Siobhan Branfield","doi":"10.1097/MOH.0000000000000918","DOIUrl":"10.1097/MOH.0000000000000918","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review summarizes current understanding of platelet-endothelial contributions to thrombosis, emphasizing molecular crosstalk [von Willebrand factor (VWF)/ADAMTS13 balance, P-selectin, platelet glycoprotein VI (GPVI), integrins, extracellular vesicles, neutrophil extracellular traps (NETs)], high-risk clinical settings, and translational advances. Highlighting GPVI-directed therapeutics, the VWF/ADAMTS13 axis in COVID-19, and opportunities and challenges for targeting the platelet-endothelial interface.</p><p><strong>Recent findings: </strong>Clinical and translational studies support the safety and potential efficacy of targeting platelet-endothelial interfaces. GPVI inhibitors (Glenzocimab, Revacept) have advanced through phase I/II studies with reassuring bleeding profiles and suggest benefit in ischemic stroke and lesion-directed settings. Direct interruption of platelet-VWF interactions (Caplacizumab) is established in immune thrombotic thrombocytopenic purpura (TTP), while studies show a persistent VWF/ADAMTS13 imbalance in severe COVID-19 and inflammatory states linked to microthrombosis and worse outcomes. Antiadhesion strategies (P-selectin blockade) and modulators of immunothrombosis (NET inhibitors, targeting extracellular vesicle) are also in evaluation.</p><p><strong>Summary: </strong>Targeting platelet-endothelial crosstalk has potential to reduce pathologic thrombosis while preserving hemostasis. Clinical proof of principle exists for focused approaches (anti-VWF in TTP; P-selectin blockade in vaso-occlusion; emerging GPVI inhibitors). Priorities are: defining disease contexts and timing where interface targeting is effective; validating biomarkers (VWF/ADAMTS13 ratio, soluble P-selectin, platelet activation signatures) for patient selection; and conducting adequately powered trials with rigorous bleeding endpoints.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"88-94"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147391759","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}
引用次数: 0
The multifaceted role of platelets in systemic sclerosis: beyond haemostasis! 血小板在系统性硬化症中的多重作用:超越止血!
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-27 DOI: 10.1097/MOH.0000000000000917
Veronica Batani, Aslihan Avanoglu Guler, Jelena Colic
{"title":"The multifaceted role of platelets in systemic sclerosis: beyond haemostasis!","authors":"Veronica Batani, Aslihan Avanoglu Guler, Jelena Colic","doi":"10.1097/MOH.0000000000000917","DOIUrl":"10.1097/MOH.0000000000000917","url":null,"abstract":"<p><strong>Purpose of review: </strong>Systemic sclerosis (SSc) is characterized by early and persistent vascular injury, immune dysregulation, and fibrosis, with a growing recognition of an excess thrombotic burden that cannot be fully explained by traditional cardiovascular risk factors. Increasing experimental and clinical evidence positions platelets as mediators at the interface of vasculopathy, inflammation, and coagulation in systemic sclerosis. This review addresses emerging platelet-driven mechanisms that extend platelet function beyond haemostasis and highlight their role as intravascular messengers capable of propagating damage across organs.</p><p><strong>Recent findings: </strong>Recent literature demonstrates that platelets in SSc exhibit a persistently activated and primed phenotype, driven by endothelial injury, aberrant platelet-collagen interactions, inflammation-mediated priming, and defective platelet clearance. Activated platelets interact dynamically with immune cells, particularly neutrophils, promoting neutrophil extracellular trap formation and immunothrombosis through pathways involving HMGB1, P-selectin-PSGL-1, and GPVI. Platelet-derived mediators, including CXCL4, serotonin, PDGF, and extracellular vesicles, enable the dissemination of inflammatory and profibrotic signals, thereby contributing to endothelial dysfunction, immune activation, and fibrotic remodelling in distant vascular beds. Clinical studies increasingly link platelet activation markers with distinct disease subsets and major organ complications.</p><p><strong>Summary: </strong>Collectively, these findings identify platelets as key orchestrators and conveyors of immunothrombosis and thromboinflammation in SSc. Improved understanding of platelet-driven signalling networks may inform risk stratification and support the development of targeted antithrombotic or immunomodulatory strategies, although robust evidence for disease-modifying antiplatelet interventions remains limited.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"95-104"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328186","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}
引用次数: 0
Membrane phospholipids in the regulation of tissue factor procoagulant function. 膜磷脂在组织因子促凝功能中的调节作用。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-18 DOI: 10.1097/MOH.0000000000000914
Shabbir A Ansari, Mohini Mendiratta, Atrayee Bhattacharya
{"title":"Membrane phospholipids in the regulation of tissue factor procoagulant function.","authors":"Shabbir A Ansari, Mohini Mendiratta, Atrayee Bhattacharya","doi":"10.1097/MOH.0000000000000914","DOIUrl":"10.1097/MOH.0000000000000914","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review is crucial because growing evidence has shifted our understanding of the regulation of tissue factor (TF) procoagulant function more towards a view that emphasizes membrane lipid remodeling as a critical determinant of TF procoagulant activity. Advances in biophysical, mechanistic, and functional studies have enabled detailed interrogation of TF-lipid interactions, necessitating an updated synthesis of current mechanistic models.</p><p><strong>Recent findings: </strong>Classical studies have established that TF exists predominantly in an encrypted, low-activity state. Recent studies have highlighted the requirement for membrane reorganization for TF procoagulant function. Phospholipid remodeling, particularly phosphatidylserine externalization and sphingomyelin hydrolysis, emerges as a central driver of TF decryption. High-resolution imaging, molecular dynamics simulations, and functional studies reveal that lipid modulation alters protein-lipid interactions, membrane curvature, and microdomain organization, thereby optimizing the spatial and conformational alignment of clotting factors.</p><p><strong>Summary: </strong>These findings underscore the role of membrane phospholipids as active regulators of TF function in both resting and pathological states. Thus, defining phospholipid-dependent TF decryption may guide future research on coagulation regulation and support the development of targeted antithrombotic strategies that selectively modulate membrane-driven TF activity.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"73-80"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328261","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}
引用次数: 0
Messengers of coagulopathy: complement-carrying extracellular vesicles in SARS-CoV-2 infection. 凝血功能的信使:SARS-CoV-2感染中携带补体的细胞外囊泡。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-27 DOI: 10.1097/MOH.0000000000000916
Apostolos Taxiarchis, Iva Pruner
{"title":"Messengers of coagulopathy: complement-carrying extracellular vesicles in SARS-CoV-2 infection.","authors":"Apostolos Taxiarchis, Iva Pruner","doi":"10.1097/MOH.0000000000000916","DOIUrl":"10.1097/MOH.0000000000000916","url":null,"abstract":"<p><strong>Purpose of review: </strong>SARS-CoV-2 disease (COVID-19) is increasingly recognized as a thromboinflammatory vascular disorder characterized by dysregulated complement activation, endothelial injury, and sustained hypercoagulability. This review examines emerging evidence that extracellular vesicles act as key intermediaries linking complement activation to coagulation in acute and postacute COVID-19 infection.</p><p><strong>Recent findings: </strong>Recent studies demonstrate that extracellular vesicles released from platelets, endothelial cells, and neutrophils are markedly increased in COVID-19 and exhibit a combined procoagulant and complement-active phenotype. Sub-lytic complement attack, particularly membrane attack complex (MAC) deposition, triggers phosphatidylserine exposure and extracellular vesicle shedding, generating vesicles that support thrombin generation and propagate complement activity in the circulation. Extracellular vesicle-associated complement components, including C1q, C3 fragments, MASP2, and preassembled MACs, promote tissue factor decryption, platelet activation, and assembly of the prothrombinase complex, establishing a self-amplifying thromboinflammatory loop. Proteomic profiling further reveals compartment-specific extracellular vesicle signatures, with systemic extracellular vesicles enriched in complement and coagulation pathways. Importantly, complement-bearing and tissue factor-bearing extracellular vesicles persist beyond acute infection and are increasingly implicated in postacute sequelae of COVID-19.</p><p><strong>Summary: </strong>Extracellular vesicles serve as mobile platforms integrating complement activation with coagulation, providing a mechanistic framework for acute and chronic immunothrombosis in COVID-19. Targeting extracellular vesicle-mediated complement-coagulation crosstalk may offer novel diagnostic and therapeutic opportunities.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"105-112"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328218","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}
引用次数: 0
Endothelial barrier disruption and contact system modulation during bacterial infection. 细菌感染期间内皮屏障破坏和接触系统调节。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-10 DOI: 10.1097/MOH.0000000000000913
Dillon J Bohinc, Sara Zalghout
{"title":"Endothelial barrier disruption and contact system modulation during bacterial infection.","authors":"Dillon J Bohinc, Sara Zalghout","doi":"10.1097/MOH.0000000000000913","DOIUrl":"10.1097/MOH.0000000000000913","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review examines how bacterial pathogens disrupt vascular barrier integrity and manipulate coagulation with a focus on endothelial signaling pathways, bacterial effectors, and contextual determinants of host-pathogen interactions. Particular attention is given to a contact activation system member, factor XII (FXII), that operates in infection not merely via coagulation but also through immune modulation and direct antimicrobial activity.</p><p><strong>Recent findings: </strong>Emerging work reveals that loss of endothelial barrier integrity arises from both inflammatory cues and pathogen-directed manipulation of junctional complexes, the glycocalyx, and cell death programs such as pyroptosis. These mechanisms are influenced by pathogen diversity, tissue-specific environments, and heterogeneity across experimental models. Studies demonstrate that FXII function is context-dependent, supporting pathogen containment through fibrin deposition in some infections, yet promoting inflammation and dissemination in others. Additionally, pathogens such as Acinetobacter baumannii directly inhibit FXII, thereby impairing immune defense and coagulation-driven containment.</p><p><strong>Summary: </strong>Therapeutic efforts now increasingly target endothelial stabilization and coagulation-immune crosstalk, yet outcomes depend on timing, infectious context, and host state. While approaches such as glycocalyx restoration, inflammasome inhibition, and FXII-based biomimetics show promise, successful intervention will likely require combination strategies that preserve host defense while limiting vascular damage. Given the diversity of host-pathogen interactions, no single therapy is expected to be universally effective.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"113-120"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328271","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}
引用次数: 0
Clinical applications of PET imaging for evaluating treatment-induced vascular toxicity in oncology. PET成像评估肿瘤治疗性血管毒性的临床应用。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-05-01 Epub Date: 2026-02-09 DOI: 10.1097/MOH.0000000000000912
Anjana Jayaraman, Mitchel R Stacy
{"title":"Clinical applications of PET imaging for evaluating treatment-induced vascular toxicity in oncology.","authors":"Anjana Jayaraman, Mitchel R Stacy","doi":"10.1097/MOH.0000000000000912","DOIUrl":"10.1097/MOH.0000000000000912","url":null,"abstract":"<p><strong>Purpose of review: </strong>Vascular toxicity resulting from cancer and its treatment remains a largely uncharacterized and minimally treated pathology. This review highlights ongoing developments and applications of PET imaging for noninvasive characterization of cancer-associated vascular toxicity and discusses the potential prognostic value of PET imaging for predicting adverse cardiovascular outcomes in patients with cancer.</p><p><strong>Recent findings: </strong>Numerous clinical investigations have used PET imaging to evaluate vascular inflammation/toxicity in patients undergoing or completing cancer therapies, including chemotherapy, immune checkpoint inhibitors, and radiation therapy. The most widely utilized PET radionuclide for noninvasively detecting vascular toxicity in clinical oncology has been fluorine-18-fluorodeoxyglucose, which has demonstrated promising associations with disease severity and clinical outcomes. Emerging radionuclides continue to be developed for targeting immune cells and may increase the sensitivity and specificity of PET imaging for detecting vascular toxicity associated with cancers and their treatment.</p><p><strong>Summary: </strong>The use of PET imaging for noninvasive detection and quantification of cancer treatment-associated vascular toxicity continues to evolve and could provide a unique approach for predicting risk of adverse cardiovascular outcomes in various forms of cancer and treatment.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":"121-127"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196070","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}
引用次数: 0
BEACH domain-containing proteins: emerging roles in hematopoiesis and immune homeostasis. 含有BEACH结构域的蛋白:在造血和免疫稳态中的新作用。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-03-17 DOI: 10.1097/MOH.0000000000000921
Abigail Hateley, Miguel Ganuza
{"title":"BEACH domain-containing proteins: emerging roles in hematopoiesis and immune homeostasis.","authors":"Abigail Hateley, Miguel Ganuza","doi":"10.1097/MOH.0000000000000921","DOIUrl":"https://doi.org/10.1097/MOH.0000000000000921","url":null,"abstract":"<p><strong>Purpose of review: </strong>BEACH-domain-containing proteins (BDCPs) are large scaffolding proteins that regulate vesicle trafficking, autophagy, and granule biogenesis. This review synthesizes recent mechanistic and clinical advances defining BDCP functions in hematopoietic stem and progenitor cell (HSPC) biology, immune regulation, and platelet function, highlighting relevance to human disease.</p><p><strong>Recent findings: </strong>Although BDCPs were initially linked to lineage-restricted hematopoietic disorders such as Chediak-Higashi syndrome and Gray platelet syndrome (GPS), emerging evidence demonstrates broader roles for BDCPs including NBEA, LRBA, LYST, and NBEAL2 in HSPC maintenance, receptor trafficking, and lineage specification. NBEA regulates NOTCH receptor turnover in HSPCs, linking vesicle dynamics to stem cell fate decisions. Recent studies provide mechanistic insights on how LRBA controls autophagy and CTLA-4 recycling, informing abatacept therapy; how NBEAL2 governs platelet α-granule biogenesis and immune homeostasis in GPS; and how LYST regulates lysosomal size and granule maturation in myeloid cells. Additionally, WDFY3, WDFY4, and WDR81 emerge as regulators of autophagy, antigen presentation, and inflammatory signaling.</p><p><strong>Summary: </strong>Collectively, BDCPs integrate vesicle trafficking, autophagy, and receptor homeostasis to coordinate hematopoietic development and immune function. Their dysfunction underlies immunological, hematologic, and inflammatory disorders, positioning BDCPs as promising translational targets.</p>","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147500798","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}
引用次数: 0
Editorial introduction. 编辑介绍。
IF 2.9 3区 医学
Current Opinion in Hematology Pub Date : 2026-03-01 Epub Date: 2026-01-29 DOI: 10.1097/MOH.0000000000000908
{"title":"Editorial introduction.","authors":"","doi":"10.1097/MOH.0000000000000908","DOIUrl":"10.1097/MOH.0000000000000908","url":null,"abstract":"","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":"33 2","pages":"v"},"PeriodicalIF":2.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146088182","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}
引用次数: 0
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