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  1. Article ; Online: Thrombin: Coagulation's master regulator of innate immunity.

    Conway, Edward M

    Journal of thrombosis and haemostasis : JTH

    2019  Volume 17, Issue 11, Page(s) 1785–1789

    MeSH term(s) Animals ; Blood Coagulation ; Humans ; Immunity, Innate ; Interleukin-1/immunology ; Interleukin-1/metabolism ; Signal Transduction ; Thrombin/immunology ; Thrombin/metabolism
    Chemical Substances Interleukin-1 ; Thrombin (EC 3.4.21.5)
    Language English
    Publishing date 2019-08-20
    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.14586
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  2. Article: Polyphosphates and Complement Activation.

    Conway, Edward M

    Frontiers in medicine

    2019  Volume 6, Page(s) 67

    Abstract: To sustain life in environments that are fraught with risks of life-threatening injury, organisms have developed innate protective strategies such that the response to wounds is rapid and localized, with the simultaneous recruitment of molecular, ... ...

    Abstract To sustain life in environments that are fraught with risks of life-threatening injury, organisms have developed innate protective strategies such that the response to wounds is rapid and localized, with the simultaneous recruitment of molecular, biochemical, and cellular pathways that limit bleeding and eliminate pathogens and damaged host cells, while promoting effective healing. These pathways are both coordinated and tightly regulated, as their over- or under-activation may lead to inadequate healing, disease, and/or demise of the host. Recent advances in our understanding of coagulation and complement, a key component of innate immunity, have revealed an intriguing linkage of the two systems. Cell-secreted polyphosphate promotes coagulation, while dampening complement activation, discoveries that are providing insights into disease mechanisms and suggesting novel therapeutic strategies.
    Language English
    Publishing date 2019-04-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2019.00067
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  3. Article ; Online: Coagulation and complement: Key innate defense participants in a seamless web.

    Pryzdial, Edward L G / Leatherdale, Alexander / Conway, Edward M

    Frontiers in immunology

    2022  Volume 13, Page(s) 918775

    Abstract: In 1969, Dr. Oscar Ratnoff, a pioneer in delineating the mechanisms by which coagulation is activated and complement is regulated, wrote, "In the study of biological processes, the accumulation of information is often accelerated by a narrow point of ... ...

    Abstract In 1969, Dr. Oscar Ratnoff, a pioneer in delineating the mechanisms by which coagulation is activated and complement is regulated, wrote, "In the study of biological processes, the accumulation of information is often accelerated by a narrow point of view. The fastest way to investigate the body's defenses against injury is to look individually at such isolated questions as how the blood clots or how complement works. We must constantly remind ourselves that such distinctions are man-made. In life, as in the legal cliché, the devices through which the body protects itself form a seamless web, unwrinkled by our artificialities." Our aim in this review, is to highlight the critical molecular and cellular interactions between coagulation and complement, and how these two major component proteolytic pathways contribute to the seamless web of innate mechanisms that the body uses to protect itself from injury, invading pathogens and foreign surfaces.
    MeSH term(s) Blood Coagulation ; Cell Communication ; Complement System Proteins/metabolism ; Humans ; Thrombosis
    Chemical Substances Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2022-08-09
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.918775
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Complement contributions to COVID-19.

    Conway, Edward M / Pryzdial, Edward L G

    Current opinion in hematology

    2022  Volume 29, Issue 5, Page(s) 259–265

    Abstract: Purpose of review: COVID-19 remains a major source of concern, particularly as new variants emerge and with recognition that patients may suffer long-term effects. Mechanisms underlying SARS-CoV-2 mediated organ damage and the associated vascular ... ...

    Abstract Purpose of review: COVID-19 remains a major source of concern, particularly as new variants emerge and with recognition that patients may suffer long-term effects. Mechanisms underlying SARS-CoV-2 mediated organ damage and the associated vascular endotheliopathy remain poorly understood, hindering new drug development. Here, we highlight selected key concepts of how the complement system, a major component of innate immunity that is dysregulated in COVID-19, participates in the thromboinflammatory response and drives the vascular endotheliopathy.
    Recent findings: Recent studies have revealed mechanisms by which complement is activated directly by SARS-CoV-2, and how the system interfaces with other innate thromboinflammatory cellular and proteolytic pathways involving platelets, neutrophils, neutrophil extracellular traps and the coagulation and kallikrein-kinin systems. With this new information, multiple potential sites for therapeutic intervention are being uncovered and evaluated in the clinic.
    Summary: Infections with SARS-CoV-2 cause damage to the lung alveoli and microvascular endothelium via a process referred to as thromboinflammation. Although not alone in being dysregulated, complement is an early player, prominent in promoting the endotheliopathy and consequential organ damage, either directly and/or via the system's complex interplay with other cellular, molecular and biochemical pathways. Delineating these critical interactions is revealing novel and promising strategies for therapeutic intervention.
    MeSH term(s) COVID-19 ; Complement System Proteins ; Extracellular Traps ; Humans ; Inflammation ; SARS-CoV-2 ; Thrombosis/etiology
    Chemical Substances Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2022-07-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000724
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    Zs.A 3703: Show issues Location:
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  5. Article ; Online: Complement-coagulation connections.

    Conway, Edward M

    Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis

    2018  Volume 29, Issue 3, Page(s) 243–251

    Abstract: Complement and coagulation are evolutionarily related proteolytic cascades in the blood that are critical for effecting an appropriate innate response to injury that limits bleeding and infection, while promoting healing. Although often viewed as ... ...

    Abstract : Complement and coagulation are evolutionarily related proteolytic cascades in the blood that are critical for effecting an appropriate innate response to injury that limits bleeding and infection, while promoting healing. Although often viewed as distinct, it has long been recognized that cross-talk likely exists between these pathways. Only recently have molecular links been established. These are providing insights that are revealing opportunities for the development of novel therapeutic strategies to better treat a wide range of thrombotic, inflammatory, immune, infectious, and malignant diseases. In this brief review, the complex relationship between complement and coagulation is highlighted, underlining some of the newly uncovered interactions, in the hopes of stimulating innovative research that will yield improvements in patient outcomes.
    MeSH term(s) Animals ; Blood Coagulation ; Complement System Proteins ; Humans ; Therapeutics
    Chemical Substances Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2018-03-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1033551-1
    ISSN 1473-5733 ; 0957-5235
    ISSN (online) 1473-5733
    ISSN 0957-5235
    DOI 10.1097/MBC.0000000000000720
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  6. Article ; Online: Biomaterial and cellular implants: foreign surfaces where immunity and coagulation meet.

    Kizhakkedathu, Jayachandran N / Conway, Edward M

    Blood

    2021  Volume 139, Issue 13, Page(s) 1987–1998

    Abstract: Exposure of blood to a foreign surface in the form of a diagnostic or therapeutic biomaterial device or implanted cells or tissue elicits an immediate, evolutionarily conserved thromboinflammatory response from the host. Primarily designed to protect ... ...

    Abstract Exposure of blood to a foreign surface in the form of a diagnostic or therapeutic biomaterial device or implanted cells or tissue elicits an immediate, evolutionarily conserved thromboinflammatory response from the host. Primarily designed to protect against invading organisms after an injury, this innate response features instantaneous activation of several blood-borne, highly interactive, well-orchestrated cascades and cellular events that limit bleeding, destroy and eliminate the foreign substance or cells, and promote healing and a return to homeostasis via delicately balanced regenerative processes. In the setting of blood-contacting synthetic or natural biomaterials and implantation of foreign cells or tissues, innate responses are robust, albeit highly context specific. Unfortunately, they tend to be less than adequately regulated by the host's natural anticoagulant or anti-inflammatory pathways, thereby jeopardizing the functional integrity of the device, as well as the health of the host. Strategies to achieve biocompatibility with a sustained return to homeostasis, particularly while the device remains in situ and functional, continue to elude scientists and clinicians. In this review, some of the complex mechanisms by which biomaterials and cellular transplants provide a "hub" for activation and amplification of coagulation and immunity, thromboinflammation, are discussed, with a view toward the development of innovative means of overcoming the innate challenges.
    MeSH term(s) Biocompatible Materials/therapeutic use ; Blood Coagulation ; Humans ; Inflammation/drug therapy ; Prostheses and Implants ; Thrombosis/drug therapy ; Thrombosis/etiology
    Chemical Substances Biocompatible Materials
    Language English
    Publishing date 2021-08-20
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020007209
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  7. Article ; Online: Sweeteners for factor H.

    Conway, Edward M

    Blood

    2016  Volume 127, Issue 22, Page(s) 2656–2658

    MeSH term(s) Complement Factor H ; Hemolytic-Uremic Syndrome ; Humans ; N-Acetylneuraminic Acid/metabolism
    Chemical Substances Complement Factor H (80295-65-4) ; N-Acetylneuraminic Acid (GZP2782OP0)
    Language English
    Publishing date 2016-06-01
    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-2016-04-708172
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  8. Article ; Online: Polyphosphates and Complement Activation

    Edward M. Conway

    Frontiers in Medicine, Vol

    2019  Volume 6

    Abstract: To sustain life in environments that are fraught with risks of life-threatening injury, organisms have developed innate protective strategies such that the response to wounds is rapid and localized, with the simultaneous recruitment of molecular, ... ...

    Abstract To sustain life in environments that are fraught with risks of life-threatening injury, organisms have developed innate protective strategies such that the response to wounds is rapid and localized, with the simultaneous recruitment of molecular, biochemical, and cellular pathways that limit bleeding and eliminate pathogens and damaged host cells, while promoting effective healing. These pathways are both coordinated and tightly regulated, as their over- or under-activation may lead to inadequate healing, disease, and/or demise of the host. Recent advances in our understanding of coagulation and complement, a key component of innate immunity, have revealed an intriguing linkage of the two systems. Cell-secreted polyphosphate promotes coagulation, while dampening complement activation, discoveries that are providing insights into disease mechanisms and suggesting novel therapeutic strategies.
    Keywords innate immunity ; thrombosis ; inflammation ; coagulation ; age-related macular degeneration ; mouse models ; Medicine (General) ; R5-920
    Language English
    Publishing date 2019-04-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: A Nuclear Attack on Thrombosis and Inflammation.

    Conway, Edward M

    Arteriosclerosis, thrombosis, and vascular biology

    2016  Volume 36, Issue 2, Page(s) 221–223

    MeSH term(s) Animals ; Carotid Stenosis/prevention & control ; DNA-Binding Proteins/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Male ; Nerve Tissue Proteins/metabolism ; Nuclear Receptor Subfamily 4, Group A, Member 1/metabolism ; Receptors, Steroid/metabolism ; Receptors, Thyroid Hormone/metabolism ; Thrombomodulin/metabolism ; Thrombosis/prevention & control
    Chemical Substances DNA-Binding Proteins ; Nerve Tissue Proteins ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Receptors, Steroid ; Receptors, Thyroid Hormone ; Thrombomodulin
    Language English
    Publishing date 2016-02
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.115.306979
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  10. Article ; Online: Is the COVID-19 thrombotic catastrophe complement-connected?

    Conway, Edward M / Pryzdial, Edward L G

    Journal of thrombosis and haemostasis : JTH

    2020  Volume 18, Issue 11, Page(s) 2812–2822

    Abstract: In December 2019, the world was introduced to a new betacoronavirus, referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for its propensity to cause rapidly progressive lung damage, resulting in high death rates. As fast as the ... ...

    Abstract In December 2019, the world was introduced to a new betacoronavirus, referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for its propensity to cause rapidly progressive lung damage, resulting in high death rates. As fast as the virus spread, it became evident that the novel coronavirus causes a multisystem disease (COVID-19) that may involve multiple organs and has a high risk of thrombosis associated with striking elevations in pro-inflammatory cytokines, D-dimer, and fibrinogen, but without disseminated intravascular coagulation. Postmortem studies have confirmed the high incidence of venous thromboembolism, but also notably revealed diffuse microvascular thrombi with endothelial swelling, consistent with a thrombotic microangiopathy, and inter-alveolar endothelial deposits of complement activation fragments. The clinicopathologic presentation of COVID-19 thus parallels that of other thrombotic diseases, such as atypical hemolytic uremic syndrome (aHUS), that are caused by dysregulation of the complement system. This raises the specter that many of the thrombotic complications arising from SARS-CoV-2 infections may be triggered and/or exacerbated by excess complement activation. This is of major potential clinical relevance, as currently available anti-complement therapies that are highly effective in protecting against thrombosis in aHUS, could be efficacious in COVID-19. In this review, we provide mounting evidence for complement participating in the pathophysiology underlying the thrombotic diathesis associated with pathogenic coronaviruses, including SARS-CoV-2. Based on current knowledge of complement, coagulation and the virus, we suggest lines of study to identify novel therapeutic targets and the rationale for clinical trials with currently available anti-complement agents for COVID-19.
    MeSH term(s) Animals ; Anticoagulants/therapeutic use ; Blood Coagulation/drug effects ; COVID-19/blood ; COVID-19/immunology ; COVID-19/virology ; Complement Activation/drug effects ; Complement Inactivating Agents/therapeutic use ; Complement System Proteins/immunology ; Host-Pathogen Interactions ; Humans ; SARS-CoV-2/immunology ; Thrombosis/blood ; Thrombosis/immunology ; Thrombosis/prevention & control ; Thrombosis/virology ; COVID-19 Drug Treatment
    Chemical Substances Anticoagulants ; Complement Inactivating Agents ; Complement System Proteins (9007-36-7)
    Keywords covid19
    Language English
    Publishing date 2020-09-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1111/jth.15050
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