Current Opinion in Hematology最新文献

Aging in the bone marrow: when hematopoiesis gets clonal. 骨髓老化：当造血获得克隆时。

IF 2.9 3区医学

Current Opinion in Hematology Pub Date : 2026-05-04 DOI: 10.1097/MOH.0000000000000928

Dawn M E Bowdish, Candice Quin

{"title":"Aging in the bone marrow: when hematopoiesis gets clonal.","authors":"Dawn M E Bowdish, Candice Quin","doi":"10.1097/MOH.0000000000000928","DOIUrl":"https://doi.org/10.1097/MOH.0000000000000928","url":null,"abstract":"Purpose of review: It has been known that the cytokine TNF (tumor necrosis factor alpha) influences hematopoiesis for decades. We now know that increases in TNF in the aging microenvironment favor the persistence and expansion of myeloid progenitors, especially those that contain mutations associated with clonal hematopoiesis of indeterminate potential (CHIP). Herein, we will examine both seminal and recent studies that have advanced our understanding of how TNF shapes hematopoietic development during aging and influences clonal dynamics in CHIP.Recent findings: Elevated levels of TNF contribute to engraftment and expansion of CHIP-mutant clones; however, there are subtle differences between the specific CHIP mutations. Sex differences in levels of TNF may contribute to differences in the frequency and types of CHIP mutations found in males and females. Anti-TNF inhibitors reduce the frequency of CHIP mutation containing clones in multiple inflammatory diseases.Summary: The elevated levels of TNF that occur with both age and chronic inflammatory conditions contribute to both myeloid skewing and CHIP. Anti-TNF drugs reduce problematic changes in myeloid hematopoiesis. Anti-TNF drugs are not an effective strategy to treat CHIP and more research is needed as to whether other anti-inflammatory strategies, including diet and exercise, are also effective.","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147846727","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

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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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

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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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

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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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 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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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":"Purpose of review: 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.Recent findings: 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.Summary: 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.","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

YY1 in hematopoietic stem cells: epigenetic regulation, chromatin architecture, and aging. YY1在造血干细胞中的作用：表观遗传调控、染色质结构和衰老。

IF 2.9 3区医学

Current Opinion in Hematology Pub Date : 2026-04-07 DOI: 10.1097/MOH.0000000000000925

Yinghua Wang, Xuan Pan

{"title":"YY1 in hematopoietic stem cells: epigenetic regulation, chromatin architecture, and aging.","authors":"Yinghua Wang, Xuan Pan","doi":"10.1097/MOH.0000000000000925","DOIUrl":"https://doi.org/10.1097/MOH.0000000000000925","url":null,"abstract":"Purpose of review: Yin Yang 1 (YY1) is a multifunctional transcription factor (TF) with established roles in lymphocyte development. More recently, its functions as a Polycomb group (PcG) protein and chromatin structural regulator in the hematopoietic system have gained increasing attention. This mini-review summarizes emerging insights into the epigenetic and architectural roles of YY1 in fetal and adult hematopoietic stem cells (HSCs), extending beyond its classical transcriptional activity. We also discuss how altered YY1 function contributes to HSC aging and hematopoietic decline.Recent findings: Recent studies show that YY1 is essential for maintaining HSC quiescence, self-renewal, and engraftment during both fetal and adult hematopoiesis. Mechanistically, YY1 regulates hematopoiesis through PcG-dependent pathways and by shaping higher-order chromatin organization. It mediates long-range chromatin interactions, cooperates with cohesin and CTCF to organize three-dimensional genome architecture, and coordinates transcriptional and metabolic programs critical for stem cell maintenance. Notably, age-associated reductions in YY1 activity are linked to functional impairment of HSCs, implicating YY1 in hematopoietic aging.Summary: YY1 acts as a TF, chromatin organizer, and PcG protein in hematopoiesis. Defining its roles in normal and aging HSCs may reveal mechanisms of hematopoietic decline and inform strategies to preserve blood system function.","PeriodicalId":55196,"journal":{"name":"Current Opinion in Hematology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147789909","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