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1.
Clin Transl Sci ; 17(4): e13784, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38563414

RESUMO

The inhibition of coagulation factor XI (FXI) presents an attractive approach for anticoagulation as it is not expected to increase the risk of clinically relevant bleeding and is anticipated to be at least as effective as currently available anticoagulants. Fesomersen is a conjugated antisense oligonucleotide that selectively inhibits the expression of FXI. The article describes three clinical studies that investigated the safety, pharmacokinetic (PK), and pharmacodynamic (PD) profiles of fesomersen after subcutaneous (s.c.) injection to healthy participants. The studies included participants from diverse ethnic backgrounds (Caucasian, Japanese, and Chinese). Fesomersen demonstrated good safety and tolerability in all three studies. No major bleeding events were observed. After single-dose s.c. injection, fesomersen was rapidly absorbed into the systemic circulation, with maximum fesomersen-equivalent (fesomersen-eq) concentrations (Cmax) in plasma observed within a few hours. After reaching Cmax, plasma fesomersen-eq concentrations declined in a biphasic fashion. The PD analyses showed that the injection of fesomersen led to dose-dependent reductions in FXI activity and increases in activated partial thromboplastin time (aPTT). The maximum observed PD effects were reached between Day 15 and 30, and FXI activity and aPTT returned to near-baseline levels by Day 90 after a single dose. The PK/PD profiles after a single injection were similar among the various ethnic groups. Collectively, the study results suggest that fesomersen has a favorable safety profile and predictable and similar PK and PD profiles across Chinese, Japanese, and Caucasian participants.


Assuntos
Fator XI , Hemorragia , Humanos , Relação Dose-Resposta a Droga , Método Duplo-Cego , Voluntários Saudáveis , Tempo de Tromboplastina Parcial , População do Leste Asiático , População Branca
2.
Rev. clín. esp. (Ed. impr.) ; 224(3): 167-177, mar. 2024. tab, graf
Artigo em Espanhol | IBECS | ID: ibc-231458

RESUMO

Antecedentes y objetivo La información proveniente de los ensayos clínicos fase 2 sugiere que los inhibidores del factor XI podrían mostrar un perfil de eficacia/seguridad más favorable que las terapias antitrombóticas actuales. El objetivo de esta revisión sistemática es analizar la evidencia disponible derivada de esos estudios. Métodos Se realizó una búsqueda bibliográfica en las bases de datos PubMed, Cochrane Library, Scopus y EMBASE, y en las plataformas de registro de ensayos clínicos Clinical Trials y Cochrane Central Register of Controlled Trials. Los resultados se publicaron según la declaración PRISMA. Resultados Se identificaron un total de 18 ensayos clínicos concluidos o en curso abordando múltiples escenarios, incluyendo fibrilación auricular, ictus, infarto de miocardio y tromboembolismo venoso. Se analizó la evidencia procedente de 8 estudios con resultados disponibles. En general, los estudios fase 2 con inhibidores del factor XI mostraron un perfil adecuado de eficacia y seguridad. El balance beneficio/riesgo fue más favorable en términos de reducción de tromboembolismo venoso en pacientes sometidos a artroplastia total de rodilla. Para esta indicación, los inhibidores del factor XI mostraron una reducción global del 50% en la tasa de complicaciones trombóticas y del 60% en la tasa de hemorragias comparado con enoxaparina. En los estudios de pacientes con fibrilación auricular, ictus e infarto de miocardio se observaron resultados más modestos. Conclusión Los inhibidores del Factor XI abren nuevas perspectivas en el tratamiento y la profilaxis antitrombótica. Los estudios fase 3 en curso permitirán definir los fármacos e indicaciones más idóneas. (AU)


Background and objective Data from phase 2 clinical trials suggest that factor XI inhibitors may exhibit a more favourable efficacy/safety profile than current antithrombotic therapies. This systematic review aims to analyze the available evidence derived from these studies. Methods A literature search in the PubMed, Cochrane Library, Scopus, EMBASE databases, and clinical trial registration platforms Clinical Trials and Cochrane Central Register of Controlled was conducted. The results were reported in accordance with the PRISMA statement. Results A total of 18 completed or ongoing clinical trials addressing multiple scenarios, including atrial fibrillation, stroke, myocardial infarction, and venous thromboembolism, were identified. Evidence from 8 studies with available results was analyzed. Overall, phase 2 studies with factor XI inhibitors demonstrated an acceptable efficacy and safety profile. The benefit-risk balance, in terms of reducing venous thromboembolism in patients undergoing total knee arthroplasty, was more favourable. For this scenario, factor XI inhibitors showed a 50% reduction in the overall rate of thrombotic complications and a 60% reduction in bleeding compared to enoxaparin. Modest results in studies involving patients with atrial fibrillation, stroke, and myocardial infarction were observed. Conclusions Factor XI inhibitors offer new prospects in antithrombotic treatment and prevention. Ongoing phase 3 studies will help define the most suitable drugs and indications. (AU)


Assuntos
Humanos , Ensaios Clínicos como Assunto , Fator XI/antagonistas & inibidores , Fibrinolíticos , Trombose/terapia , Hemorragia
3.
Rev Clin Esp (Barc) ; 224(3): 167-177, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38309621

RESUMO

INTRODUCTION AND OBJECTIVE: Data from phase 2 clinical trials suggest that factor XI inhibitors may exhibit a more favorable efficacy/safety profile compared to current antithrombotic therapies. The aim of this systematic review is to analyze the available evidence derived from these studies. METHODS: A literature search in the PubMed, Cochrane Library, Scopus, EMBASE databases, and clinical trial registration platforms Clinical Trials and Cochrane Central Register of Controlled was conducted. In accordance with the PRISMA statement, results were reported. RESULTS: A total of 18 completed or ongoing clinical trials addressing multiple scenarios, including atrial fibrillation, stroke, myocardial infarction, and venous thromboembolism, were identified. Evidence from 8 studies with available results was analyzed. Phase 2 studies with factor XI inhibitors, overall, demonstrated an acceptable efficacy and safety profile. The benefit-risk balance, in terms of reducing venous thromboembolism in patients undergoing total knee arthroplasty, was more favorable. For this scenario, factor XI inhibitors showed a 50% reduction in the overall rate of thrombotic complications and a 60% reduction in the rate of bleeding compared to enoxaparin. Modest results in studies involving patients with atrial fibrillation, stroke, and myocardial infarction were observed. CONCLUSIONS: Factor XI inhibitors offer new prospects in antithrombotic treatment and prophylaxis. Ongoing phase 3 studies will help define the most suitable drugs and indications.


Assuntos
Fibrilação Atrial , Infarto do Miocárdio , Acidente Vascular Cerebral , Tromboembolia Venosa , Humanos , Anticoagulantes/uso terapêutico , Fibrinolíticos/uso terapêutico , Tromboembolia Venosa/tratamento farmacológico , Tromboembolia Venosa/prevenção & controle , Fator XI , Fibrilação Atrial/tratamento farmacológico , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/prevenção & controle , Infarto do Miocárdio/tratamento farmacológico , Infarto do Miocárdio/prevenção & controle
5.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 36(1): 16-22, 2024 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-38404266

RESUMO

Anticoagulation therapy stands as a key treatment for thrombotic diseases. The consequential bleeding risk tied to existing anticoagulation methods significantly impacts patient prognosis. In the intensive care unit (ICU), patients often necessitate organ support, leading to the inevitable placement of artificial devices in blood vessels, thereby requiring anticoagulation treatment to avert clot formation that might impede organ support. Nevertheless, these patients commonly encounter a heightened risk of bleeding. Hemophilia B, identified in 1953, manifests as a deficiency in coagulation factor XI (FXI), which focused people's perspective on the endogenous coagulation pathway, that is, the contact pathway. Upon interaction between the surface of artificial devices and FXII, FXII activates, subsequently triggering FXI and initiating the "coagulation cascade" within the contact pathway. Inhibitors targeting the contact pathway encompass two primary categories: FXII inhibitors and FXI inhibitors, capable of impeding this process. This article reviews the role of FXII and FXI in activating the contact pathway, seeking to illuminate their contributions to thrombus formation. By listing the relatively mature drugs and their indications, clinicians are familiar with this new anticoagulant.


Assuntos
Fator XII , Trombose , Humanos , Fator XII/metabolismo , Fator XII/farmacologia , Coagulação Sanguínea , Fator XI/metabolismo , Fator XI/farmacologia , Trombose/tratamento farmacológico , Anticoagulantes/uso terapêutico
6.
J Cardiothorac Surg ; 19(1): 40, 2024 Feb 02.
Artigo em Inglês | MEDLINE | ID: mdl-38303013

RESUMO

BACKGROUND: Coagulation factor XI deficiency is an autosomal recessive hereditary disease with a low incidence. It usually occurs after surgery or trauma; Esophageal cancer is a common malignant tumor of the digestive tract in China. But so far, surgery-based comprehensive treatment of esophageal cancer still dominates. CASE PRESENTATION: We report a case of an Asian patient with XI factor deficiency and lower esophageal squamous cell carcinoma who was admitted to our hospital recently. After active preoperative preparation, the operation was successfully performed, and there was no obvious abnormal bleeding during and after the operation. CONCLUSIONS: Coagulation factor XI deficiency is a relatively rare disease, and patients with the disease will face a greater risk of bleeding during the perioperative period. The encouraging perioperative outcome enables us to have a deeper understanding of surgical treatment strategies for patients with Coagulation factor XI deficiency.


Assuntos
Neoplasias Esofágicas , Carcinoma de Células Escamosas do Esôfago , Deficiência do Fator XI , Humanos , Neoplasias Esofágicas/complicações , Neoplasias Esofágicas/cirurgia , Carcinoma de Células Escamosas do Esôfago/complicações , Carcinoma de Células Escamosas do Esôfago/cirurgia , Fator XI , Deficiência do Fator XI/complicações , Hemorragia/etiologia , Masculino , Idoso
9.
Curr Diabetes Rev ; 20(1): e210323214817, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-36944622

RESUMO

INTRODUCTION: Maturity-onset diabetes of the young (MODY) is a rare disease due to a single gene mutation that affects several family members in most cases. The Krüppel-like factor 11 (KLF11) gene mutation is associated with decreased insulin sensitivity to high glucose levels. KLF 11 has been implicated in the pathogenesis of MODY type 7 but given its low prevalence, prolonged subclinical period, and the emergence of new information, doubts are raised about its association. METHODS: A literature search of the PubMed, Scopus, and EBSCO databases was performed. The terms "Diabetes Mellitus, Type 2/genetics", "Mason-Type Diabetes" , "Maturity-Onset diabetes of the young", "KLF11 protein, human", and "Maturity-Onset Diabetes of the Young, Type 7" were used"., "Diagnosis" The search selection was not standardized. RESULTS: The KLF1 mutation is rare and represents <1% of the mutations associated with monogenic diabetes. Its isolation in European family lines in the first studies and the emergence of new variants pose new diagnostic challenges. This article reviews the definition, epidemiology, pathophysiology, diagnosis, and treatment of MODY type 7. CONCLUSION: MODY type 7 diabetes represents a rare form of monogenic diabetes with incomplete penetrance. Given its rarity, its association with impaired glucose metabolism has been questioned. Strict evaluation of glycemic control and the appearance of microvascular complications are key areas in the follow-up of patients diagnosed with MODY 7. More studies will be required to characterize the population with KLF11 mutation and clarify its correlation with MODY.


Assuntos
Diabetes Mellitus Tipo 2 , Fator XI , Humanos , Fator XI/genética , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/diagnóstico , Mutação , Insulina , Proteínas Repressoras/genética , Proteínas Reguladoras de Apoptose/genética
11.
Blood Coagul Fibrinolysis ; 35(1): 32-36, 2024 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-38051652

RESUMO

To examine real-life clinical data regarding hereditary factor XI (FXI) deficiency from a secondary care centre. Retrospective review of clinical records for every FXI:C 0.7 IU/ml or less reported from 2012 to 2020. Seventy-nine patients were included. Six (7.6%) had a severe deficiency (FXI:C <0.2 IU/ml). Only 55 (69.6%) patients were referred to the Haemostasis Centre. Among them, six (15%) were subsequently not identified at increased haemorrhagic risk before a surgical/obstetrical procedure. Thirty-three (41.8%) experienced at least one bleeding event, minor (25 patients) and/or major (16 patients). Minor bleedings were predominantly spontaneous and more frequent in women, major events were mainly provoked. No correlation was found between FXI:C and risk of bleeding ( P  = 0.9153). Lower FXI:C, but not a positive bleeding history, was related with higher likelihood of being referred to the Haemostasis Centre ( P  = 0.0333). Hereditary FXI deficiency prevalence is likely underestimated, real-life clinical practices outside reference centres could be suboptimal.


Assuntos
Deficiência do Fator XI , Fator XI , Feminino , Humanos , Fator XI/genética , Deficiência do Fator XI/epidemiologia , Deficiência do Fator XI/genética , Hemorragia/complicações , Itália/epidemiologia , Doenças Negligenciadas/complicações , Estudos Retrospectivos , Masculino
12.
Arterioscler Thromb Vasc Biol ; 44(1): 290-299, 2024 01.
Artigo em Inglês | MEDLINE | ID: mdl-37970718

RESUMO

BACKGROUND: Despite the ubiquitous utilization of central venous catheters in clinical practice, their use commonly provokes thromboembolism. No prophylactic strategy has shown sufficient efficacy to justify routine use. Coagulation factors FXI (factor XI) and FXII (factor XII) represent novel targets for device-associated thrombosis, which may mitigate bleeding risk. Our objective was to evaluate the safety and efficacy of an anti-FXI mAb (monoclonal antibody), gruticibart (AB023), in a prospective, single-arm study of patients with cancer receiving central line placement. METHODS: We enrolled ambulatory cancer patients undergoing central line placement to receive a single dose of gruticibart (2 mg/kg) administered through the venous catheter within 24 hours of placement and a follow-up surveillance ultrasound at day 14 for evaluation of catheter thrombosis. A parallel, noninterventional study was used as a comparator. RESULTS: In total, 22 subjects (n=11 per study) were enrolled. The overall incidence of catheter-associated thrombosis was 12.5% in the interventional study and 40.0% in the control study. The anti-FXI mAb, gruticibart, significantly prolonged the activated partial thromboplastin time in all subjects on day 14 compared with baseline (P<0.001). Gruticibart was well tolerated and without infusion reactions, drug-related adverse events, or clinically relevant bleeding. Platelet flow cytometry demonstrated no difference in platelet activation following administration of gruticibart. T (thrombin)-AT (antithrombin) and activated FXI-AT complexes increased following central line placement in the control study, which was not demonstrated in our intervention study. CRP (C-reactive protein) did not significantly increase on day 14 in those who received gruticibart, but it did significantly increase in the noninterventional study. CONCLUSIONS: FXI inhibition with gruticibart was well tolerated without any significant adverse or bleeding-related events and resulted in a lower incidence of catheter-associated thrombosis on surveillance ultrasound compared with the published literature and our internal control study. These findings suggest that targeting FXI could represent a safe intervention to prevent catheter thrombosis. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04465760.


Assuntos
Neoplasias , Trombose , Humanos , Fator XI/metabolismo , Estudos Prospectivos , Trombose/etiologia , Trombose/prevenção & controle , Trombose/tratamento farmacológico , Hemorragia/induzido quimicamente , Cateteres/efeitos adversos , Neoplasias/tratamento farmacológico , Neoplasias/complicações
13.
Vasc Med ; 29(1): 85-92, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-37947131

RESUMO

During the past decade, direct oral anticoagulants (DOACs) have advanced and simplified the prevention and treatment of venous thromboembolism (VTE). However, there remains a high incidence of bleeds, which calls for agents that have a reduced risk of bleeding. Factor XI (FXI) deficiency is associated with lower rates of venous thrombosis and stroke compared to the general population with a lower risk of bleeding. In conjunction with this, phase 2 studies have demonstrated safety and the potential for reduced thrombotic events with FXI inhibitors as compared to currently available medications. The aim of this review is to summarize key data on the clinical pharmacology of FXI, the latest developments in clinical trials of FXI inhibitors, and to describe the efficacy and safety profiles of FXI inhibitors for the prevention of venous and arterial thromboembolism.


Assuntos
Tromboembolia Venosa , Trombose Venosa , Humanos , Anticoagulantes/efeitos adversos , Fator XI/uso terapêutico , Trombose Venosa/diagnóstico , Trombose Venosa/tratamento farmacológico , Trombose Venosa/prevenção & controle , Hemorragia/induzido quimicamente , Hemorragia/tratamento farmacológico , Tromboembolia Venosa/diagnóstico , Tromboembolia Venosa/tratamento farmacológico , Tromboembolia Venosa/prevenção & controle
15.
J Thromb Haemost ; 22(1): 199-212, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37751848

RESUMO

BACKGROUND: Cancer-associated thrombosis is a frequent complication in patients with malignancies. While factor XI (FXI)/FXIa inhibition is efficacious in preventing postoperative venous thromboembolism, its role in tumor cell-induced coagulation is less defined. OBJECTIVES: We thus aimed to provide mechanistic insights into FXI/FXIa inhibition in tumor cell-induced coagulation activation. METHODS: Procoagulant activity (PCA) of 4 different tissue factor (TF) expressing tumor cell lines was analyzed by single-stage clotting and thrombin generation assay in the presence of a FXIa inhibitor, BMS-262084 (BMS), an inhibitory FXI antibody (anti-FXI), or peak and trough concentrations of rivaroxaban or tinzaparin. Further, tumor cell-induced platelet aggregation was recorded. Recombinant human TF served as positive control. RESULTS: Although BMS and anti-FXI potently inhibited FXIa amidolytic activity, both inhibitors efficiently mitigated recombinant human TF- and tumor cell-induced fibrin clot formation and platelet aggregation only in the presence of low TF PCA. The anticoagulant effects showed an inverse correlation with the magnitude of cellular TF PCA expression. Similarly, BMS markedly interfered with tumor cell-induced thrombin generation, with the most prominent effects on peak and total thrombin. In addition, anticoagulant effects of FXIa inhibition by 10 µM BMS were in a similar range to those obtained by 600 nM rivaroxaban and 1.6 µM tinzaparin at low TF PCA levels. However, rivaroxaban and tinzaparin also exerted marked anticoagulant activity at high TF PCA levels. CONCLUSION: Our findings indicate that FXI/FXIa inhibition interferes with tumor cell-induced coagulation activation only at low TF PCA expression levels, a finding with potential implications for future in vivo studies.


Assuntos
Fator XI , Neoplasias , Humanos , Fator XI/metabolismo , Rivaroxabana , Tinzaparina , Trombina/metabolismo , Tromboplastina/metabolismo , Anticoagulantes/farmacologia , Neoplasias/tratamento farmacológico , Fator XIa/metabolismo
16.
J Thromb Haemost ; 22(1): 225-237, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37813198

RESUMO

BACKGROUND: In plasma, high molecular weight kininogen (HK) is either free or bound to prekallikrein (PK) or factor (F) XI (FXI). During contact activation, HK is thought to anchor PK and FXI to surfaces, facilitating their conversion to the proteases plasma kallikrein and FXIa. Mice lacking HK have normal hemostasis but are resistant to injury-induced arterial thrombosis. OBJECTIVES: To identify amino acids on the HK-D6 domain involved in PK and FXI binding and study the importance of the HK-PK and HK-FXI interactions to coagulation. METHODS: Twenty-four HK variants with alanine replacements spanning residues 542-613 were tested in PK/FXI binding and activated partial thromboplastin time clotting assays. Surface-induced FXI and PK activation in plasma were studied in the presence or absence of HK. Kng1-/- mice lacking HK were supplemented with human or murine HK and tested in an arterial thrombosis model. RESULTS: Overlapping binding sites for PK and FXI were identified in the HK-D6 domain. HK variants with defects only in FXI binding corrected the activated partial thromboplastin time of HK-deficient plasma poorly compared to a variant defective only in PK-binding. In plasma, HK deficiency appeared to have a greater deleterious effect on FXI activation than PK activation. Human HK corrected the defect in arterial thrombus formation in HK-deficient mice poorly due to a specific defect in binding to mouse FXI. CONCLUSION: Clinical observations indicate FXI is required for hemostasis, while HK is not. Yet, the HK-FXI interaction is required for contact activation-induced clotting in vitro and in vivo suggesting an important role in thrombosis and perhaps other FXI-related activities.


Assuntos
Cininogênio de Alto Peso Molecular , Trombose , Animais , Humanos , Camundongos , Cininogênio de Alto Peso Molecular/metabolismo , Fator XI/metabolismo , Pré-Calicreína/metabolismo , Coagulação Sanguínea
17.
J Thromb Thrombolysis ; 57(3): 402-407, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38145433

RESUMO

Cerebral venous sinus thrombosis (CVST) has no identified cause in 15% of cases. Elevated factors (F) VIII and FXI have been associated with thromboembolism, but data on CVST are limited. We hypothesized that elevated plasma FVIII and FXI predispose to first and recurrent CVST. In 50 CVST survivors aged < 60 years, following anticoagulant cessation and in 50 controls, we determined plasma FVIII and FXI, along with fibrin clot properties: lysis time, permeability, maximum D-dimer (D-Dmax), and maximum rate of D-dimer increase (D-Drate). We recorded CVST recurrence during a follow-up of 58.5 (55.0-60.0) months. Plasma FVIII was 22.7% higher in CVST than in controls, with elevated FVIII > 150% in 13 (26%) vs. 4 (8%) patients, respectively (p = 0.02). Median FXI tended to be higher in CVST vs. controls (110.5 [99.0-117-0]% vs. 104.5 [97.0-116.0]%, p = 0.07), while FXI > 120% was observed more commonly in the former group (12 [24%] vs. 4 [8%], respectively, p = 0.03). Patients with FVIII > 150% were less likely to achieve complete recanalization compared with the remainder (2 [15.4%] vs. 28 [75.7%], respectively; p < 0.001). Eight patients (16%) experienced CVST recurrence. They had higher baseline FXI, but not FVIII, as compared with the remainder (125.5 [114.5-140.0]% vs. 107.5 [102.0-117.0]%, respectively, p = 0.01). Patients with FXI > 120% were four times more likely to have recurrent CVST (5 [62.5%] vs. 7 [16.7%], respectively; p = 0.01). Plasma FXI > 120% could represent a novel risk factor for first and recurrent CVST. Given advances in anti-FXI agents, CVST might be another indication for this emerging treatment.


Assuntos
Fator XI , Trombose dos Seios Intracranianos , Humanos , Estudos de Coortes , Fatores de Risco , Fibrina , Trombose dos Seios Intracranianos/etiologia
19.
Curr Opin Hematol ; 31(1): 32-38, 2024 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-37694771

RESUMO

PURPOSE OF REVIEW: This review summarizes the pathophysiology and potential therapeutic options for treatment of multiple sclerosis, a common neuronal demyelinating disorder affecting 2.2 million people worldwide. As an autoimmune disorder, multiple sclerosis is associated with neuroinflammation and increased permeability of the blood-brain barrier (BBB), although the cause linking multiple sclerosis with compromised barrier function remains ill-defined. It has been previously shown that coagulation factors, including thrombin and fibrin, exacerbate the inflammatory processes and permeability of the BBB. RECENT FINDINGS: Increased levels of the coagulation factor (F) XII have been found in patients presenting with relapsing-remitting multiple sclerosis, with a deleterious role for FXII being validated in murine model of multiple sclerosis, experimental autoimmune encephalitis (EAE). Recent work has uncovered a role for the major substrate activated by FXII and thrombin, FXI, in the disorder of EAE. The study found that pharmacological targeting of FXI decreased clinical symptoms, lymphocyte invasion, and white matter destruction in a multiple sclerosis model. SUMMARY: This review emphasizes the role of FXII and FXI in regulating barrier function and the immune response in neuroinflammation. These new findings broaden the potential for therapeutic utility of FXI inhibitors beyond thrombosis to include neuroinflammatory diseases associated with compromised BBB function, including multiple sclerosis.


Assuntos
Fator XI , Esclerose Múltipla , Humanos , Animais , Camundongos , Fator XII , Doenças Neuroinflamatórias , Trombina , Esclerose Múltipla/tratamento farmacológico
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