We are analyzing https://link.springer.com/article/10.1186/s12959-015-0048-y.

Title:
Contact pathway of coagulation and inflammation | Thrombosis Journal
Description:
The contact system, also named as plasma kallikrein-kinin system, consists of three serine proteinases: coagulation factors XII (FXII) and XI (FXI), and plasma prekallikrein (PK), and the nonenzymatic cofactor high molecular weight kininogen (HK). This system has been investigated actively for more than 50 years. The components of this system and their interactions have been elucidated from in vitro experiments, which indicates that this system is prothrombotic by activating intrinsic pathway, and proinflammatory by producing bioactive peptide bradykinin. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. In the last 10 years, our understanding of the contact system, particularly its biology and (patho)physiology has greatly increased through investigations using gene-modified animal models. In this review we will describe a revitalized view of the contact system as a critical (patho)physiologic mediator of coagulation and inflammation.
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Keywords {🔍}

contact, system, activation, pubmed, plasma, article, google, scholar, cas, bradykinin, fxii, role, factor, mice, arthritis, coagulation, thrombosis, cells, formation, inflammatory, disease, inflammation, deficiency, patients, cell, pathway, kininogen, central, endothelial, tissue, model, activated, kallikrein, human, blood, proteins, kks, surface, intrinsic, receptors, thrombus, pmcid, xii, surfaces, protein, thromb, kallikreinkinin, prekallikrein, increased, ibd,

Topics {✒️}

arg-pro-pro-gly-phe-ser-pro-phe-arg circulating plasmin-a2-antiplasmin complexes low-molecular-weight kininogen anti-collagen antibody-induced arthritis desamino d-arginine vasopressin including angiotensin-converting enzyme blood-brain barrier damage peptide-based inhibitor pck carotid artery occlusion recombinant infestin-4-based inhibitor homing receptor c-x cellular-based microbicidal systems fxia-driven thrombin generation continuous fxii-dependent formation open access license tissue-type plasminogen activator curli-expressing escherichia coli dela cadena ra thrombosis search search gene-modified animal models bk-mediated vascular leakage article download pdf dextran sulfate sodium tissue factor-initiated coagulation kunitz-type protein expressed nonenzymatic cofactor hk surface-coated tissue factor plasma kallikrein-kinin system kallikrein-kininogen system activation oversulfated chondroitin sulfate collagen-induced arthritis model vascular biology modulator urokinase-type pa plasma host-defense systems pro-inflammatory mediators fxii-gene-deficient mice cell membrane-mediated assembly kallikrein-kinin system activation privacy choices/manage cookies anti-fibrinolytic factor high plasma levels pro-inflammatory effect [4] tick ixodes ricinus inhibitory monoclonal antibody govers-riemslag jw gpcr-mediated pathways bacteria resembles protein-binding bradykinin-derived peptides propagate venous thrombosis misfolded protein aggregates

Schema {🗺️}

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         headline:Contact pathway of coagulation and inflammation
         description:The contact system, also named as plasma kallikrein-kinin system, consists of three serine proteinases: coagulation factors XII (FXII) and XI (FXI), and plasma prekallikrein (PK), and the nonenzymatic cofactor high molecular weight kininogen (HK). This system has been investigated actively for more than 50 years. The components of this system and their interactions have been elucidated from in vitro experiments, which indicates that this system is prothrombotic by activating intrinsic pathway, and proinflammatory by producing bioactive peptide bradykinin. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. In the last 10 years, our understanding of the contact system, particularly its biology and (patho)physiology has greatly increased through investigations using gene-modified animal models. In this review we will describe a revitalized view of the contact system as a critical (patho)physiologic mediator of coagulation and inflammation.
         datePublished:2015-05-06T00:00:00Z
         dateModified:2015-05-06T00:00:00Z
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            Inflammation
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            Autoimmune disease
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            Cardiology
            Hematology
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      headline:Contact pathway of coagulation and inflammation
      description:The contact system, also named as plasma kallikrein-kinin system, consists of three serine proteinases: coagulation factors XII (FXII) and XI (FXI), and plasma prekallikrein (PK), and the nonenzymatic cofactor high molecular weight kininogen (HK). This system has been investigated actively for more than 50 years. The components of this system and their interactions have been elucidated from in vitro experiments, which indicates that this system is prothrombotic by activating intrinsic pathway, and proinflammatory by producing bioactive peptide bradykinin. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. In the last 10 years, our understanding of the contact system, particularly its biology and (patho)physiology has greatly increased through investigations using gene-modified animal models. In this review we will describe a revitalized view of the contact system as a critical (patho)physiologic mediator of coagulation and inflammation.
      datePublished:2015-05-06T00:00:00Z
      dateModified:2015-05-06T00:00:00Z
      pageStart:1
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      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12959-015-0048-y
      keywords:
         Contact system
         Coagulation
         Inflammation
         Platelet
         Infection
         Autoimmune disease
         Vascular biology
         Angiology
         Cardiology
         Hematology
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Person:
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            name:Temple University School of Medicine
            address:
               name:The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, USA

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