CIDeRplusGeneral Information:
| Id: | 12,080 |
| Diseases: |
COVID-19
Cardiovascular disease |
| Mammalia | |
| review | |
| Reference: | Henry BM et al.(2020) Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis Clin. Chim. Acta 507: 167-173 [PMID: 32348783] |
Interaction Information:
| Comment | Hyperinflammation promotes endothelial cell activation and endothelial dysfunction, which may induce a prothrombotic state. |
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Formal Description Interaction-ID: 118584 |
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| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118596 |
increases_activity of |
| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118598 |
increases_activity of |
| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118637 |
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| Drugbank entries | Show/Hide entries for F2 |
| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118639 |
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| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118640 |
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| Drugbank entries | Show/Hide entries for F2 |
| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118642 |
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| Comment | The coagulation system is activated through the tissue factor (extrinsic) pathway and is amplified by the formerly known intrinsic pathway (now called ‚Äúthrombin burst‚ÄĚ). The thrombin burst finally converges to activate the ‚Äėcommon‚Äô pathway, where Factor Va (FVa) and FXa converts prothrombin into thrombin. |
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Formal Description Interaction-ID: 118643 |
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| Drugbank entries | Show/Hide entries for F2 |
| Comment | Thrombin converts fibrinogen into fibrin, which is stabilized into the clot by FXIIIa activity. |
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Formal Description Interaction-ID: 118644 |
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| Comment | Thrombin converts fibrinogen into fibrin, which is stabilized into the clot by FXIIIa activity. |
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Formal Description Interaction-ID: 118645 |
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| Comment | Thrombin converts fibrinogen into fibrin, which is stabilized into the clot by FXIIIa activity. |
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Formal Description Interaction-ID: 118646 |
complex/PPI Fibrinogen increases_quantity of complex/PPI Fibrin |
| Comment | Thrombin converts fibrinogen into fibrin, which is stabilized into the clot by FXIIIa activity. |
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Formal Description Interaction-ID: 118647 |
complex/PPI Fibrin increases_quantity of complex/PPI Fibrin clot |
| Comment | Thrombin converts fibrinogen into fibrin, which is stabilized into the clot by FXIIIa activity. |
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Formal Description Interaction-ID: 118648 |
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| Drugbank entries | Show/Hide entries for F13A1 |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118649 |
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| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118650 |
gene/protein increases_quantity of complex/PPI Plasmin |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118651 |
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| Drugbank entries | Show/Hide entries for PLAT |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118652 |
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| Drugbank entries | Show/Hide entries for PLAT or PLG |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118653 |
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| Drugbank entries | Show/Hide entries for PLAU |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118654 |
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| Drugbank entries | Show/Hide entries for PLAU or PLG |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 118655 |
complex/PPI Plasmin decreases_quantity of complex/PPI Fibrin clot |
| Comment | Both tPA (PLAT) and uPA (PLAU) are inhibited by plasminogen activator inhibitor-1 (PAI-1). Balance between tPA/uPA and PAI-1 ensures balanced homeostasis. |
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Formal Description Interaction-ID: 118656 |
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| Drugbank entries | Show/Hide entries for SERPINE1 or PLAU |
| Comment | Both tPA (PLAT) and uPA (PLAU) are inhibited by plasminogen activator inhibitor-1 (PAI-1). Balance between tPA/uPA and PAI-1 ensures balanced homeostasis. |
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Formal Description Interaction-ID: 118657 |
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| Drugbank entries | Show/Hide entries for SERPINE1 or PLAT |
| Comment | In acute respiratory distress syndrome (ARDS), the the balance between tPA/uPA and PAI-1 is disturbed, with excessive PAI-1 resulting in relative hypofibrinolysis leading to fibrin deposition in the alveoli and perialveolar capillary microthrombosis. ARDS is induced in COVID-19 patients. |
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Formal Description Interaction-ID: 118658 |
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| Drugbank entries | Show/Hide entries for SERPINE1 |
| Comment | In acute respiratory distress syndrome (ARDS), the the balance between tPA/uPA and PAI-1 is disturbed, with excessive PAI-1 resulting in relative hypofibrinolysis leading to fibrin deposition in the alveoli and perialveolar capillary microthrombosis. ARDS is induced in COVID-19 patients. |
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Formal Description Interaction-ID: 118659 |
disease COVID-19 increases_activity of phenotype acute respiratory distress syndrome |
| Comment | In acute respiratory distress syndrome (ARDS), the the balance between tPA/uPA and PAI-1 is disturbed, with excessive PAI-1 resulting in relative hypofibrinolysis leading to fibrin deposition in the alveoli and perialveolar capillary microthrombosis. ARDS is induced in COVID-19 patients. |
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Formal Description Interaction-ID: 118660 |
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| Comment | The extrinsic pathway is initiated by tissue factor (TF, F3), which in inflammatory states is expressed by activated endothelial cells and monocyte/macrophages. |
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Formal Description Interaction-ID: 118662 |
tissue/cell line increases_activity of |
| Comment | The extrinsic pathway is initiated by tissue factor (TF, F3), which in inflammatory states is expressed by activated endothelial cells and monocyte/macrophages. |
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Formal Description Interaction-ID: 118663 |
tissue/cell line increases_activity of |
| Comment | The extrinsic pathway is initiated by tissue factor (TF, F3), which in inflammatory states is expressed by activated endothelial cells and monocyte/macrophages. |
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Formal Description Interaction-ID: 118711 |
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| Drugbank entries | Show/Hide entries for F3 |
| Comment | The extrinsic pathway is initiated by tissue factor (TF, F3), which in inflammatory states is expressed by activated endothelial cells and monocyte/macrophages. |
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Formal Description Interaction-ID: 118712 |
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| Drugbank entries | Show/Hide entries for F3 |
| Comment | Platelets have well-known roles in coagulation, but they also exert pro-inflammatory effects. |
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Formal Description Interaction-ID: 118713 |
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| Comment | Platelets have well-known roles in coagulation, but they also exert pro-inflammatory effects. |
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Formal Description Interaction-ID: 118714 |
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| Comment | Activation of platelets leads to changes in their shape and release of their stored granules. Platelet alpha granules contain immunostimulatory molecules which are involved in activation and recruitment of neutrophiles (PMNs) and monocytes/macrophages (M√ł), including platelet factor 4 (CXCL4), proplatelet basic protein, neutrophil-activating peptide-2 (CXCL7) and stromal cell-derived factor. In addition, activated platelets are also an important source of pro-inflammatory IL-1beta. |
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Formal Description Interaction-ID: 118715 |
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| Comment | Activation of platelets leads to changes in their shape and release of their stored granules. Platelet alpha granules contain immunostimulatory molecules which are involved in activation and recruitment of neutrophiles (PMNs) and monocytes/macrophages (M√ł), including platelet factor 4 (CXCL4), proplatelet basic protein, neutrophil-activating peptide-2 (CXCL7) and stromal cell-derived factor. In addition, activated platelets are also an important source of pro-inflammatory IL-1beta. |
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Formal Description Interaction-ID: 118716 |
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| Comment | Activation of platelets leads to changes in their shape and release of their stored granules. Platelet alpha granules contain immunostimulatory molecules which are involved in activation and recruitment of neutrophiles (PMNs) and monocytes/macrophages (M√ł), including platelet factor 4 (CXCL4), proplatelet basic protein, neutrophil-activating peptide-2 (CXCL7) and stromal cell-derived factor. In addition, activated platelets are also an important source of pro-inflammatory IL-1beta. |
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Formal Description Interaction-ID: 118717 |
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| Drugbank entries | Show/Hide entries for PF4 |
| Comment | Activation of platelets leads to changes in their shape and release of their stored granules. Platelet alpha granules contain immunostimulatory molecules which are involved in activation and recruitment of neutrophiles (PMNs) and monocytes/macrophages (M√ł), including platelet factor 4 (CXCL4), proplatelet basic protein, neutrophil-activating peptide-2 (CXCL7) and stromal cell-derived factor. In addition, activated platelets are also an important source of pro-inflammatory IL-1beta. |
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Formal Description Interaction-ID: 118718 |
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| Drugbank entries | Show/Hide entries for PPBP |
| Comment | Activation of platelets leads to changes in their shape and release of their stored granules. Platelet alpha granules contain immunostimulatory molecules which are involved in activation and recruitment of neutrophiles (PMNs) and monocytes/macrophages (M√ł), including platelet factor 4 (CXCL4), proplatelet basic protein, neutrophil-activating peptide-2 (CXCL7) and stromal cell-derived factor. In addition, activated platelets are also an important source of pro-inflammatory IL-1beta. |
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Formal Description Interaction-ID: 118719 |
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| Drugbank entries | Show/Hide entries for IL1B |
| Comment | A mouse model of SARS demonstrated that dysregulated complement activation contributed to lung damage and systemic inflammation. Complement activation induces a cascade of events, culminating in generation of pleiotropic bioactive molecules, such as C3a, C5a and membrane attack complex. |
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Formal Description Interaction-ID: 118720 |
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| Comment | A mouse model of SARS demonstrated that dysregulated complement activation contributed to lung damage and systemic inflammation. Complement activation induces a cascade of events, culminating in generation of pleiotropic bioactive molecules, such as C3a, C5a and membrane attack complex. |
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Formal Description Interaction-ID: 118721 |
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| Comment | A mouse model of SARS demonstrated that dysregulated complement activation contributed to lung damage and systemic inflammation. Complement activation induces a cascade of events, culminating in generation of pleiotropic bioactive molecules, such as C3a, C5a and membrane attack complex. |
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Formal Description Interaction-ID: 118722 |
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| Comment | C3a and C5a exert a multitude of pro-inflammatory effects. In addition, they exert pro-thrombotic effects through activation of platelets and endothelial cells, as well as increasing tissue factor and von Willebrand factor (VWF) expression. |
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Formal Description Interaction-ID: 118723 |
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| Comment | C3a and C5a exert a multitude of pro-inflammatory effects. In addition, they exert pro-thrombotic effects through activation of platelets and endothelial cells, as well as increasing tissue factor and von Willebrand factor (VWF) expression. |
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Formal Description Interaction-ID: 118724 |
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| Comment | C3a and C5a exert a multitude of pro-inflammatory effects. In addition, they exert pro-thrombotic effects through activation of platelets and endothelial cells, as well as increasing tissue factor and von Willebrand factor (VWF) expression. |
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Formal Description Interaction-ID: 118725 |
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| Drugbank entries | Show/Hide entries for VWF |
| Comment | MASP-1 and MASP-2, two proteins of the complement system, also contribute to the generation of a hypercoagulable state, by converting prothrombin to thrombin and fibrinogen to fibrin. |
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Formal Description Interaction-ID: 118726 |
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| Comment | MASP-1 and MASP-2, two proteins of the complement system, also contribute to the generation of a hypercoagulable state, by converting prothrombin to thrombin and fibrinogen to fibrin. |
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Formal Description Interaction-ID: 118727 |
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| Drugbank entries | Show/Hide entries for MASP2 |
| Comment | MASP-1 and MASP-2, two proteins of the complement system, also contribute to the generation of a hypercoagulable state, by converting prothrombin to thrombin and fibrinogen to fibrin. |
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Formal Description Interaction-ID: 118728 |
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| Comment | MASP-1 and MASP-2, two proteins of the complement system, also contribute to the generation of a hypercoagulable state, by converting prothrombin to thrombin and fibrinogen to fibrin. |
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Formal Description Interaction-ID: 118729 |
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| Drugbank entries | Show/Hide entries for MASP2 |
| Comment | Fibrin clots are broken down by plasmin, in a process called fibrinolysis, initiated by two proteins that convert plasminogen to plasmin, tissue plasminogen activator (tPA, PLAT) and urokinase plasminogen activator (uPA, PLAU). |
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Formal Description Interaction-ID: 126984 |
complex/PPI Plasmin decreases_quantity of complex/PPI Fibrin |