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  1. Article ; Online: Heat shock protein 47 and venous thrombosis: letting sleeping bears lie.

    Grover, Steven P / Mackman, Nigel / Bendapudi, Pavan K

    Journal of thrombosis and haemostasis : JTH

    2023  Volume 21, Issue 10, Page(s) 2648–2652

    MeSH term(s) Animals ; Humans ; HSP47 Heat-Shock Proteins ; Ursidae ; Venous Thrombosis
    Chemical Substances HSP47 Heat-Shock Proteins
    Language English
    Publishing date 2023-07-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1016/j.jtha.2023.07.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5805: Show issues Location:
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  2. Article: Anticoagulant SERPINs: Endogenous Regulators of Hemostasis and Thrombosis.

    Grover, Steven P / Mackman, Nigel

    Frontiers in cardiovascular medicine

    2022  Volume 9, Page(s) 878199

    Abstract: Appropriate activation of coagulation requires a balance between procoagulant and anticoagulant proteins in blood. Loss in this balance leads to hemorrhage and thrombosis. A number of endogenous anticoagulant proteins, such as antithrombin and heparin ... ...

    Abstract Appropriate activation of coagulation requires a balance between procoagulant and anticoagulant proteins in blood. Loss in this balance leads to hemorrhage and thrombosis. A number of endogenous anticoagulant proteins, such as antithrombin and heparin cofactor II, are members of the serine protease inhibitor (SERPIN) family. These SERPIN anticoagulants function by forming irreversible inhibitory complexes with target coagulation proteases. Mutations in SERPIN family members, such as antithrombin, can cause hereditary thrombophilias. In addition, low plasma levels of SERPINs have been associated with an increased risk of thrombosis. Here, we review the biological activities of the different anticoagulant SERPINs. We further consider the clinical consequences of SERPIN deficiencies and insights gained from preclinical disease models. Finally, we discuss the potential utility of engineered SERPINs as novel therapies for the treatment of thrombotic pathologies.
    Language English
    Publishing date 2022-05-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2022.878199
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: "High plasma levels of C1-inhibitor are associated with lower risk of future venous thromboembolism": reply.

    Grover, Steven P / Brækkan, Sigrid K / Mackman, Nigel / Hansen, John-Bjarne

    Journal of thrombosis and haemostasis : JTH

    2023  Volume 21, Issue 10, Page(s) 2993–2995

    MeSH term(s) Humans ; Venous Thromboembolism/diagnosis ; Venous Thromboembolism/drug therapy ; Complement C1 Inhibitor Protein
    Chemical Substances Complement C1 Inhibitor Protein
    Language English
    Publishing date 2023-10-26
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1016/j.jtha.2023.07.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Description of the first mutation in the human tissue factor gene associated with a bleeding tendency.

    Grover, Steven P / Mackman, Nigel

    Journal of thrombosis and haemostasis : JTH

    2020  Volume 19, Issue 1, Page(s) 3–6

    MeSH term(s) Blood Coagulation Disorders ; Hemorrhagic Disorders ; Hemostasis ; Humans ; Mutation ; Thromboplastin/genetics
    Chemical Substances Thromboplastin (9035-58-9)
    Language English
    Publishing date 2020-11-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1111/jth.15151
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  5. Article ; Online: Tissue factor in atherosclerosis and atherothrombosis.

    Grover, Steven P / Mackman, Nigel

    Atherosclerosis

    2020  Volume 307, Page(s) 80–86

    Abstract: Atherosclerosis is a chronic inflammatory disease that is characterized by the formation of lipid rich plaques in the wall of medium to large sized arteries. Atherothrombosis represents the terminal manifestation of this pathology in which ... ...

    Abstract Atherosclerosis is a chronic inflammatory disease that is characterized by the formation of lipid rich plaques in the wall of medium to large sized arteries. Atherothrombosis represents the terminal manifestation of this pathology in which atherosclerotic plaque rupture or erosion triggers the formation of occlusive thrombi. Occlusion of arteries and resultant tissue ischemia in the heart and brain causes myocardial infarction and stroke, respectively. Tissue factor (TF) is the receptor for the coagulation protease factor VIIa, and formation of the TF:factor VIIa complex triggers blood coagulation. TF is expressed at high levels in atherosclerotic plaques by both macrophage-derived foam cells and vascular smooth muscle cells, as well as extracellular vesicles derived from these cells. Importantly, TF mediated activation of coagulation is critically important for arterial thrombosis in the setting of atherosclerotic disease. The major endogenous inhibitor of the TF:factor VIIa complex is TF pathway inhibitor 1 (TFPI-1), which is also present in atherosclerotic plaques. In mouse models, increased or decreased expression of TFPI-1 has been found to alter atherosclerosis. This review highlights the contribution of TF-dependent activation of coagulation to atherthrombotic disease.
    MeSH term(s) Animals ; Atherosclerosis ; Blood Coagulation ; Mice ; Plaque, Atherosclerotic ; Thromboplastin ; Thrombosis
    Chemical Substances Thromboplastin (9035-58-9)
    Language English
    Publishing date 2020-07-03
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2020.06.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 226: Show issues Location:
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  6. Article ; Online: "Hereditary angioedema is associated with an increased risk of venous thromboembolism": reply.

    Grover, Steven P / Sundler Björkman, Linda / Egesten, Arne / Moll, Stephan / Mackman, Nigel

    Journal of thrombosis and haemostasis : JTH

    2023  Volume 21, Issue 1, Page(s) 180–182

    MeSH term(s) Humans ; Angioedemas, Hereditary ; Venous Thromboembolism/diagnosis ; Venous Thromboembolism/complications ; Complement C1 Inhibitor Protein
    Chemical Substances Complement C1 Inhibitor Protein
    Language English
    Publishing date 2023-01-25
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1016/j.jtha.2022.10.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: How useful are ferric chloride models of arterial thrombosis?

    Grover, Steven P / Mackman, Nigel

    Platelets

    2019  Volume 31, Issue 4, Page(s) 432–438

    Abstract: The ferric chloride models of arterial thrombosis are useful tools with which to investigate the cellular and molecular mechanisms that contribute to arterial thrombosis. Recent insights have, however, revealed the complex and multifaceted mechanism by ... ...

    Abstract The ferric chloride models of arterial thrombosis are useful tools with which to investigate the cellular and molecular mechanisms that contribute to arterial thrombosis. Recent insights have, however, revealed the complex and multifaceted mechanism by which ferric chloride induces thrombus formation. Here, we discuss the strengths and weaknesses of the ferric chloride models of arterial thrombosis. Particular focus is given to the phenotypes of different knockout mice in the ferric chloride models and how these compare to other models with independent modes of initiation. Further, we discuss the relevance of the ferric chloride models to the human pathology of atherothrombotic disease.
    MeSH term(s) Animals ; Anticoagulants/pharmacology ; Anticoagulants/therapeutic use ; Blood Platelets/pathology ; Carotid Artery Thrombosis/chemically induced ; Carotid Artery Thrombosis/metabolism ; Chlorides/metabolism ; Chlorides/toxicity ; Disease Models, Animal ; Erythrocytes/metabolism ; Ferric Compounds/metabolism ; Ferric Compounds/toxicity ; Humans ; Mice ; Mice, Knockout
    Chemical Substances Anticoagulants ; Chlorides ; Ferric Compounds ; ferric chloride (U38V3ZVV3V)
    Language English
    Publishing date 2019-10-13
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1034283-7
    ISSN 1369-1635 ; 0953-7104
    ISSN (online) 1369-1635
    ISSN 0953-7104
    DOI 10.1080/09537104.2019.1678119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2888: Show issues Location:
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  8. Article ; Online: Intrinsic Pathway of Coagulation and Thrombosis.

    Grover, Steven P / Mackman, Nigel

    Arteriosclerosis, thrombosis, and vascular biology

    2019  Volume 39, Issue 3, Page(s) 331–338

    Abstract: Activation of the intrinsic pathway of coagulation contributes to the pathogenesis of arterial and venous thrombosis. Critical insights into the involvement of intrinsic pathway factors have been derived from the study of gene-specific knockout animals ... ...

    Abstract Activation of the intrinsic pathway of coagulation contributes to the pathogenesis of arterial and venous thrombosis. Critical insights into the involvement of intrinsic pathway factors have been derived from the study of gene-specific knockout animals and targeted inhibitors. Importantly, preclinical studies have indicated that targeting components of this pathway, including FXI (factor XI), FXII, and PKK (prekallikrein), reduces thrombosis with no significant effect on protective hemostatic pathways. This review highlights the advances made from studying the intrinsic pathway using gene-specific knockout animals and inhibitors in models of arterial and venous thrombosis. Development of inhibitors of activated FXI and FXII may reduce thrombosis with minimal increases in bleeding compared with current anticoagulant drugs.
    MeSH term(s) Animals ; Anticoagulants/adverse effects ; Anticoagulants/pharmacology ; Anticoagulants/therapeutic use ; Bleeding Time ; Blood Coagulation/drug effects ; Blood Coagulation/physiology ; Blood Coagulation Factors/antagonists & inhibitors ; Blood Coagulation Factors/genetics ; Blood Coagulation Factors/physiology ; Disease Models, Animal ; Drug Design ; Enzyme Activation ; Hemorrhage/chemically induced ; Humans ; Mice, Knockout ; Primates ; Rabbits ; Rats ; Thrombosis/drug therapy ; Thrombosis/epidemiology ; Thrombosis/physiopathology ; Thrombosis/prevention & control
    Chemical Substances Anticoagulants ; Blood Coagulation Factors
    Language English
    Publishing date 2019-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.118.312130
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Tissue factor expression, extracellular vesicles, and thrombosis after infection with the respiratory viruses influenza A virus and coronavirus.

    Mackman, Nigel / Grover, Steven P / Antoniak, Silvio

    Journal of thrombosis and haemostasis : JTH

    2021  Volume 19, Issue 11, Page(s) 2652–2658

    Abstract: Tissue factor (TF) is induced in a variety of cell types during viral infection, which likely contributes to disseminated intravascular coagulation and thrombosis. TF-expressing cells also release TF-positive extracellular vesicles (EVs) into the ... ...

    Abstract Tissue factor (TF) is induced in a variety of cell types during viral infection, which likely contributes to disseminated intravascular coagulation and thrombosis. TF-expressing cells also release TF-positive extracellular vesicles (EVs) into the circulation that can be measured using an EVTF activity assay. This review summarizes studies that analyze TF expression, TF-positive EVs, activation of coagulation, and thrombosis after infection with influenza A virus (IAV) and coronaviruses (CoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), SARS-CoV, and Middle East respiratory syndrome CoV (MERS-CoV). The current pandemic of coronavirus disease 2019 (COVID-19) is caused by infection with SARS-CoV-2. Infection of mice with IAV increased TF expression in lung epithelial cells as well as increased EVTF activity and activation of coagulation in the bronchoalveolar lavage fluid (BALF). Infection of mice with MERS-CoV, SARS-CoV, and SARS-CoV-2 also increased lung TF expression. Single-cell RNA sequencing analysis on the BALF from severe COVID-19 patients revealed increased TF mRNA expression in epithelial cells. TF expression was observed in peripheral blood mononuclear cells infected with SARS-CoV. TF was also expressed by peripheral blood mononuclear cells, monocytes in platelet-monocyte aggregates, and neutrophils isolated from COVID-19 patients. Elevated circulating EVTF activity was observed in severe IAV and COVID-19 patients. Importantly, EVTF activity was associated with mortality in severe IAV patients and with plasma D-dimer, severity, thrombosis, and mortality in COVID-19 patients. These studies strongly suggest that increased TF expression in patients infected with IAV and pathogenic CoVs contributes to thrombosis.
    MeSH term(s) Animals ; COVID-19 ; Extracellular Vesicles ; Humans ; Influenza A virus ; Leukocytes, Mononuclear ; Mice ; SARS-CoV-2 ; Thromboplastin ; Thrombosis
    Chemical Substances Thromboplastin (9035-58-9)
    Language English
    Publishing date 2021-09-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1111/jth.15509
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Neutrophils, NETs, and immunothrombosis.

    Grover, Steven P / Mackman, Nigel

    Blood

    2018  Volume 132, Issue 13, Page(s) 1360–1361

    MeSH term(s) Animals ; Mice ; Neutrophil Activation ; Neutrophils ; Receptors, Interleukin-8B ; Signal Transduction ; Venous Thrombosis
    Chemical Substances Receptors, Interleukin-8B
    Language English
    Publishing date 2018-09-21
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-08-868067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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