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      Endothelial cell control of thrombosis

      research-article
      , ,
      BMC Cardiovascular Disorders
      BioMed Central
      Endothelial cells, Thrombosis, Blood coagulation

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          Abstract

          Hemostasis encompasses a set of tightly regulated processes that govern blood clotting, platelet activation, and vascular repair. Upon vascular injury, the hemostatic system initiates a series of vascular events and activates extravascular receptors that act in concert to seal off the damage. Blood clotting is subsequently attenuated by a plethora of inhibitors that prevent excessive clot formation and eventual thrombosis. The endothelium which resides at the interface between the blood and surrounding tissues, serves an integral role in the hemostatic system. Depending on specific tissue needs and local stresses, endothelial cells are capable of evoking either antithrombotic or prothrombotic events. Healthy endothelial cells express antiplatelet and anticoagulant agents that prevent platelet aggregation and fibrin formation, respectively. In the face of endothelial dysfunction, endothelial cells trigger fibrin formation, as well as platelet adhesion and aggregation. Finally, endothelial cells release pro-fibrinolytic agents that initiate fibrinolysis to degrade the clot. Taken together, a functional endothelium is essential to maintain hemostasis and prevent thrombosis. Thus, a greater understanding into the role of the endothelium can provide new avenues for exploration and novel therapies for the management of thromboembolisms.

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          Most cited references120

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          Evolving functions of endothelial cells in inflammation.

          Inflammation is usually analysed from the perspective of tissue-infiltrating leukocytes. Microvascular endothelial cells at a site of inflammation are both active participants in and regulators of inflammatory processes. The properties of endothelial cells change during the transition from acute to chronic inflammation and during the transition from innate to adaptive immunity. Mediators that act on endothelial cells also act on leukocytes and vice versa. Consequently, many anti-inflammatory therapies influence the behaviour of endothelial cells and vascular therapeutics influence inflammation. This Review describes the functions performed by endothelial cells at each stage of the inflammatory process, emphasizing the principal mediators and signalling pathways involved and the therapeutic implications.
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            Thrombin signalling and protease-activated receptors.

            S Coughlin (2000)
            How does the coagulation protease thrombin regulate cellular behaviour? The protease-activated receptors (PARs) provide one answer. In concert with the coagulation cascade, these receptors provide an elegant mechanism linking mechanical information in the form of tissue injury or vascular leakage to cellular responses. Roles for PARs are beginning to emerge in haemostasis and thrombosis, inflammation, and perhaps even blood vessel development.
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              Phenotypic heterogeneity of the endothelium: II. Representative vascular beds.

              Endothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the second of a 2-part review on the phenotypic heterogeneity of blood vessel endothelial cells. The first part discusses the scope, the underlying mechanisms, and the diagnostic and therapeutic implications of phenotypic heterogeneity. Here, these principles are applied to an understanding of organ-specific phenotypes in representative vascular beds including arteries and veins, heart, lung, liver, and kidney. The goal is to underscore the importance of site-specific properties of the endothelium in mediating homeostasis and focal vascular pathology, while at the same time emphasizing the value of approaching the endothelium as an integrated system.
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                Author and article information

                Contributors
                YauJ@smh.ca
                teohh@smh.ca
                1-416-864-5997 , vermasu@smh.ca
                Journal
                BMC Cardiovasc Disord
                BMC Cardiovasc Disord
                BMC Cardiovascular Disorders
                BioMed Central (London )
                1471-2261
                19 October 2015
                19 October 2015
                2015
                : 15
                : 130
                Affiliations
                [ ]Division of Cardiac Surgery, St. Michael’s Hospital, Suite 8-003, Bond Wing, 30 Bond St., Toronto, ON M5B 1W8 Canada
                [ ]Divisions of Endocrinology & Metabolism, Keenan Research Centre for Biomedical Science at St. Michael’s Hospital, Toronto, ON Canada
                [ ]Department of Surgery, University of Toronto, Toronto, ON Canada
                Article
                124
                10.1186/s12872-015-0124-z
                4617895
                26481314
                2fe1c643-04c3-4437-a888-a0c3d5a967ee
                © Yau et al. 2015

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 11 May 2015
                : 9 October 2015
                Categories
                Review
                Custom metadata
                © The Author(s) 2015

                Cardiovascular Medicine
                endothelial cells,thrombosis,blood coagulation
                Cardiovascular Medicine
                endothelial cells, thrombosis, blood coagulation

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