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Journal articles on the topic 'Coagulation cascade'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

GREEN, David. "Coagulation cascade." Hemodialysis International 10, S2 (2006): S2—S4. http://dx.doi.org/10.1111/j.1542-4758.2006.00119.x.

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2

Olah, Zsolt, Zsuzsanna Bereczky, Mariann Szarvas, and Zoltan Boda. "Coagulation: cascade!" Lancet 378, no. 9792 (2011): 740. http://dx.doi.org/10.1016/s0140-6736(11)60875-1.

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3

Amour, A., M. Bird, L. Chaudry, J. Deadman, D. Hayes, and C. Kay. "General considerations for proteolytic cascades." Biochemical Society Transactions 32, no. 1 (2004): 15–16. http://dx.doi.org/10.1042/bst0320015.

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Proteases are involved in the regulation of a wide variety of essential physiological processes, often by participating in a highly orchestrated sequence of events termed a ‘proteolytic cascade’. Four major proteolytic cascades with disease relevance are candidates for therapeutic intervention, namely caspase-mediated apoptosis, blood coagulation, the matrix metalloproteinase cascade and the complement cascade. Understanding the various steps involved in the functioning of a cascade is key to deciding possible points of intervention for the design of potential drug molecules. This brief review

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4

HOFFMAN, Maureane, Zhi Hong MENG, Harold R. ROBERTS, and Dougald M. MONROE. "Rethinking the Coagulation Cascade." Japanese Journal of Thrombosis and Hemostasis 16, no. 1 (2005): 70–81. http://dx.doi.org/10.2491/jjsth.16.70.

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5

Schenone, Monica, Barbara C. Furie, and Bruce Furie. "The blood coagulation cascade." Current Opinion in Hematology 11, no. 4 (2004): 272–77. http://dx.doi.org/10.1097/01.moh.0000130308.37353.d4.

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6

Monroe, Dougald M., and Maureane Hoffman. "The Coagulation Cascade in Cirrhosis." Clinics in Liver Disease 13, no. 1 (2009): 1–9. http://dx.doi.org/10.1016/j.cld.2008.09.014.

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7

Hoffman, Maureane. "Remodeling the Blood Coagulation Cascade." Journal of Thrombosis and Thrombolysis 16, no. 1/2 (2003): 17–20. http://dx.doi.org/10.1023/b:thro.0000014588.95061.28.

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8

Wang, Ling, Julie Bastarache, and Lorraine Ware. "The Coagulation Cascade in Sepsis." Current Pharmaceutical Design 14, no. 19 (2008): 1860–69. http://dx.doi.org/10.2174/138161208784980581.

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9

Nicolle, AL, KL Talks, and JP Hanley. "Congenital and acquired bleeding problems in elderly patients." Reviews in Clinical Gerontology 15, no. 1 (2005): 9–26. http://dx.doi.org/10.1017/s0959259805001735.

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Bleeding in elderly patients is most commonly due to an underlying structural problem or an acquired coagulopathy. Occasionally, previously asymptomatic congenital bleeding disorders may present at an advanced age. When considering the possible causes of a clinical bleeding problem, the coagulation cascade is still a good starting-point. However, it is important to realize that the traditional model of the coagulation cascade has been superceded by the concept of a ‘coagulation network’. This updated model recognizes the importance of tissue factor in the initiation of coagulation. Despite the

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Yang, Zhangsheng, Milomir O. Simovic, Bin Liu, et al. "Indices of complement activation and coagulation changes in trauma patients." Trauma Surgery & Acute Care Open 7, no. 1 (2022): e000927. http://dx.doi.org/10.1136/tsaco-2022-000927.

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ObjectivesEarly complementopathy and coagulopathy are shown often after trauma. However, the prevalence of any interplay between complement cascade (ComC) and coagulation cascade (CoaC) after trauma remains unclear. This study intended to explore whether complement-coagulation crosstalk exists, which may provide a reliable guide to clinical implications in trauma patients.MethodsThis single-center cohort study of trauma patients enrolled 100 patients along with 20 healthy volunteers. Blood samples from patients were collected at admission, 45, 90, 135 minutes, and 18 hours after admission. Dem

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11

Aronovich, Anna, Yaniv Nur, Elias Shezen, et al. "A novel role for factor VIII and thrombin/PAR1 in regulating hematopoiesis and its interplay with the bone structure." Blood 122, no. 15 (2013): 2562–71. http://dx.doi.org/10.1182/blood-2012-08-447458.

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Key PointsThe coagulation cascade via the factor VIII/thrombin/PAR1 axis regulates HSC maintenance. The coagulation cascade via factor VIII/thrombin/PAR1 axis regulates a reciprocal interplay between HSCs and the dynamic bone structure.

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12

Chambers, R. C., and G. J. Laurent. "Coagulation cascade proteases and tissue fibrosis." Biochemical Society Transactions 30, no. 2 (2002): 194–200. http://dx.doi.org/10.1042/bst0300194.

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Fibrotic disorders of the liver, kidney and lung are associated with excessive deposition of extracellular matrix proteins and ongoing coagulation-cascade activity. In addition to their critical roles in blood coagulation, thrombin and the immediate upstream coagulation proteases, Factors Xa and VIIa, influence numerous cellular responses that may play critical roles in subsequent inflammatory and tissue repair processes in vascular and extra-vascular compartments. The cellular effects of these proteases are mediated via proteolytic activation of a novel family of cell-surface receptors, the p

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Chambers, R. C., D. C. J. Howell, O. P. Blanc-Brude, and G. J. Laurent. "Coagulation cascade proteases and tissue fibrosis." Biochemical Society Transactions 30, no. 1 (2002): A16. http://dx.doi.org/10.1042/bst030a016a.

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14

Görlach, Agnes. "Redox Regulation of the Coagulation Cascade." Antioxidants & Redox Signaling 7, no. 9-10 (2005): 1398–404. http://dx.doi.org/10.1089/ars.2005.7.1398.

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15

Nicholson, Andrew C., and David P. Hajjar. "Viral activation of the coagulation cascade." American Heart Journal 138, no. 5 (1999): S461—S464. http://dx.doi.org/10.1016/s0002-8703(99)70275-9.

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16

Anglés-Cano, Eduardo, and Marie-Claude Guillin. "ANTIPHOSPHOLIPID ANTIBODIES AND THE COAGULATION CASCADE." Rheumatic Disease Clinics of North America 27, no. 3 (2001): 573–86. http://dx.doi.org/10.1016/s0889-857x(05)70221-0.

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17

Johari, Vandita, and Chandravathi Loke. "Brief Overview of the Coagulation Cascade." Disease-a-Month 58, no. 8 (2012): 421–23. http://dx.doi.org/10.1016/j.disamonth.2012.04.004.

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18

Roberts, Harold R., and Jay N. Lozier. "New Perspectives on the Coagulation Cascade." Hospital Practice 27, no. 1 (1992): 97–112. http://dx.doi.org/10.1080/21548331.1992.11705345.

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19

Pant, Asmita, Anna K. Kopec, and James P. Luyendyk. "Role of the blood coagulation cascade in hepatic fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 2 (2018): G171—G176. http://dx.doi.org/10.1152/ajpgi.00402.2017.

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Liver is the primary source of numerous proteins that are critical for normal function of the blood coagulation cascade. Because of this, diseases of the liver, particularly when affiliated with severe complications like cirrhosis, are associated with abnormalities of blood clotting. Although conventional interpretation has inferred cirrhosis as a disorder of uniform bleeding risk, it is now increasingly appreciated as a disease wherein the coagulation cascade is precariously rebalanced. Moreover, prothrombotic risk factors are also associated with a more rapid progression of fibrosis in human

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20

Schastlivtsev, I. V., K. V. Lobastov, S. N. Tsaplin, and D. S. Mkrtychev. "Modern view on hemostasis system: cell theory." Medical Council, no. 16 (October 9, 2019): 72–77. http://dx.doi.org/10.21518/2079-701x-2019-16-72-77.

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For many years, there has been no model capable of explaining the complex processes of interaction between various bloodclotting factors leading to a stop of bleeding. One of the most successful models able to partially reflect the mechanisms of hemostasis for a long time was the cascade theory. The cascade model perfectly explains the processes occurring during coagulation in vitro, but was completely inadequate in attempts to evaluate the processes occurring in vivo. A significant drawback of the cascade model is the impossibility to trace the interaction of cells carrying the tissue factor,

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21

Hong, Seung-No, Yu-Lian Zhang, Chae-Seo Rhee, and Dong-Young Kim. "Probable Roles of Coagulation Cascade and Fibrinolysis System in the Development of Allergic Rhinitis." American Journal of Rhinology & Allergy 33, no. 2 (2018): 137–44. http://dx.doi.org/10.1177/1945892418816015.

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Background Dysregulation of the coagulation cascade and fibrinolysis system may play an etiologic role in many diseases. Allergic diseases such as bronchial asthma, atopic dermatitis, and conjunctivitis are also associated with fibrin accumulation caused by a change in hemostasis. However, only a few studies have dealt with the relationship between allergic rhinitis (AR) and the coagulation system. Objective We investigated the difference of coagulation and fibrinolysis cascade components between an AR mouse model and a control mice. Methods BALB/c mice were sensitized and challenged with oval

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22

Vojacek, Jan F. "Should We Replace the Terms Intrinsic and Extrinsic Coagulation Pathways With Tissue Factor Pathway?" Clinical and Applied Thrombosis/Hemostasis 23, no. 8 (2016): 922–27. http://dx.doi.org/10.1177/1076029616673733.

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Present review highlights some new aspects of the role of individual components of blood coagulation process and proposes a modified concept of hemocoagulation cascade. The role of FXII in the initiation of the so-called intrinsic coagulation system is currently questioned. Its role has been recently demonstrated mainly in the thrombus propagation and final stabilization together with factors XI and XIII. The edited concept underlines the common part of the tissue factor (TF) in the initiation of both the intrinsic and extrinsic pathways of the coagulation system and therefore may make it not

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23

Strohbach, Anne, and Raila Busch. "Predicting the In Vivo Performance of Cardiovascular Biomaterials: Current Approaches In Vitro Evaluation of Blood-Biomaterial Interactions." International Journal of Molecular Sciences 22, no. 21 (2021): 11390. http://dx.doi.org/10.3390/ijms222111390.

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The therapeutic efficacy of a cardiovascular device after implantation is highly dependent on the host-initiated complement and coagulation cascade. Both can eventually trigger thrombosis and inflammation. Therefore, understanding these initial responses of the body is of great importance for newly developed biomaterials. Subtle modulation of the associated biological processes could optimize clinical outcomes. However, our failure to produce truly blood compatible materials may reflect our inability to properly understand the mechanisms of thrombosis and inflammation associated with biomateri

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24

Antoniak, Silvio, and Nigel Mackman. "Multiple roles of the coagulation protease cascade during virus infection." Blood 123, no. 17 (2014): 2605–13. http://dx.doi.org/10.1182/blood-2013-09-526277.

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Abstract The coagulation cascade is activated during viral infections. This response may be part of the host defense system to limit spread of the pathogen. However, excessive activation of the coagulation cascade can be deleterious. In fact, inhibition of the tissue factor/factor VIIa complex reduced mortality in a monkey model of Ebola hemorrhagic fever. Other studies showed that incorporation of tissue factor into the envelope of herpes simplex virus increases infection of endothelial cells and mice. Furthermore, binding of factor X to adenovirus serotype 5 enhances infection of hepatocytes

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25

Diosdado, Alicia, Fernando Simón, Rodrigo Morchón, and Javier González-Miguel. "Dirofilaria immitis possesses molecules with anticoagulant properties in its excretory/secretory antigens." Parasitology 147, no. 5 (2020): 559–65. http://dx.doi.org/10.1017/s0031182020000104.

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AbstractDirofilaria immitis is a parasitic nematode that survives in the circulatory system of suitable hosts for many years, causing the most severe thromboembolisms when simultaneous death of adult worms occurs. The two main mechanisms responsible for thrombus formation in mammals are the activation and aggregation of platelets and the generation of fibrin through the coagulation cascade. The aim of this work was to study the anticoagulant potential of excretory/secretory antigens from D. immitis adult worms (DiES) on the coagulation cascade of the host. Anticoagulant and inhibition assays r

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26

Bernard, Aline M., and Gordon R. Bernard. "The Immune Response: Targets for the Treatment of Severe Sepsis." International Journal of Inflammation 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/697592.

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The clinical process of severe sepsis is characterized by extreme inflammation interlinked with potent stimulation of the coagulation cascade often followed by a state of relative immune paralysis. In this paper, we will review many of the potential therapies directed at various steps along the inflammatory cascade from modulation of inflammatory mediators eliciting the immune response, alteration of the host's immune response in both a stimulatory and depressive manner, and taming the overexuberant coagulation response triggered by the fierce coagulation-inflammation cycle. Finally, we will d

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27

ROHRER, MICHAEL J., and ANITA M. NATALE. "Effect of hypothermia on the coagulation cascade." Critical Care Medicine 20, no. 10 (1992): 1402–5. http://dx.doi.org/10.1097/00003246-199210000-00007.

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ROHRER, M. J., and A. M. NATALE. "Effect of Hypothermia on the Coagulation Cascade." Survey of Anesthesiology 37, no. 4 (1993): 184. http://dx.doi.org/10.1097/00132586-199308000-00003.

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29

Woodruff, Rebecca S., and Bruce A. Sullenger. "Modulation of the Coagulation Cascade Using Aptamers." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 10 (2015): 2083–91. http://dx.doi.org/10.1161/atvbaha.115.300131.

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30

Davie, Earl W., Kazuo Fujikawa, and Walter Kisiel. "The coagulation cascade: initiation, maintenance, and regulation." Biochemistry 30, no. 43 (1991): 10363–70. http://dx.doi.org/10.1021/bi00107a001.

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31

McCulloch, Scott. "Effect of hypothermia on the coagulation cascade." Annals of Emergency Medicine 22, no. 3 (1993): 620. http://dx.doi.org/10.1016/s0196-0644(05)81963-8.

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32

Foley, Jonathan H., and Edward M. Conway. "Gas6 gains entry into the coagulation cascade." Blood 121, no. 4 (2013): 570–71. http://dx.doi.org/10.1182/blood-2012-11-468678.

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33

Ernoehazy, W. S. "Effect of hypothermia on the coagulation cascade." Journal of Emergency Medicine 11, no. 3 (1993): 365–66. http://dx.doi.org/10.1016/0736-4679(93)90069-j.

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34

Febrianti, Ika Kurnia, Andani Eka Putra, Raveinal, and Aisyah Elliyanti. "Transcriptomic Analysis of Coagulation Gene Expression in COVID-19 Patients." International Journal on Advanced Science, Engineering and Information Technology 14, no. 6 (2024): 2045–52. https://doi.org/10.18517/ijaseit.14.6.20019.

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The immunopathogenesis of COVID-19 infection is reported to begin with the entry of the SARS-CoV-2 virus into the human body through droplets, entering the lungs, and binding to the ACE-2 receptor. Meanwhile, activated macrophages stimulate an immune and inflammatory response, activating the coagulation cascade. This activation in COVID-19 patients can exacerbate the condition and may result in acute respiratory distress syndrome (ARDS). The coagulation cascade is influenced by the expression of related genes, including F3, F5, F8, F12, F13A1, VWF, THBD, PROC, PROCR, PROS1, SERPINE1, A2M, and

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35

Faqihi, Fahimeh, Marcus A. Stoodley, and Lucinda S. McRobb. "The Evolution of Safe and Effective Coaguligands for Vascular Targeting and Precision Thrombosis of Solid Tumors and Vascular Malformations." Biomedicines 9, no. 7 (2021): 776. http://dx.doi.org/10.3390/biomedicines9070776.

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In cardiovascular and cerebrovascular biology, control of thrombosis and the coagulation cascade in ischemic stroke, myocardial infarction, and other coagulopathies is the focus of significant research around the world. Ischemic stroke remains one of the largest causes of death and disability in developed countries. Preventing thrombosis and protecting vessel patency is the primary goal. However, utilization of the body’s natural coagulation cascades as an approach for targeted destruction of abnormal, disease-associated vessels and tissues has been increasing over the last 30 years. This vasc

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Ren, Xuanrong, and Qinghui Fu. "C3AR1 is a regulatory factor associated with coagulation cascade and inflammation in sepsis." Medicine 103, no. 11 (2024): e37519. http://dx.doi.org/10.1097/md.0000000000037519.

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Sepsis is a leading cause of mortality in intensive care units. Sepsis is associated with activation of the coagulation cascade and inflammation. The aim of this study was to identify coagulation-related genes in sepsis that may provide translational potential therapeutic targets. The datasets GSE28750, GSE95233, and GSE65682 were downloaded from the gene expression omnibus database. Consensus-weighted gene co-expression network analysis (WGCNA) was used to identify sepsis modules. Gene set enrichment analysis was used to identify genes enriched in the coagulation cascade. The value of hub-gen

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37

Davie, Earl W. "Introduction to the blood coagulation cascade and cloning of blood coagulation factors." Journal of Protein Chemistry 5, no. 4 (1986): 247–53. http://dx.doi.org/10.1007/bf01025423.

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38

Embi Bs, Abraham A. "ENERGY DETECTION IN THE FORM OF LIGHT RADIATION AT END OF HUMAN BLOOD COAGULATION CASCADE- THE OPTICAL ABSORPTION OF WATER VS. FIBRIN BURST ENERGY RELEASE." International Journal of Research -GRANTHAALAYAH 7, no. 9 (2019): 200–212. http://dx.doi.org/10.29121/granthaalayah.v7.i9.2019.602.

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The human blood coagulation cascade had been extensively researched from a biochemistry and molecular perspective. The purpose of this manuscript is to introduce a biophysical phenomenon detected via optical microscopy at the end of the human blood coagulation cascade. This could be described as a sudden energy event in the form of light radiation observed once blood tissue movement stops being attracted to metal iron filings or carbon based graphite particles used as sentinels. Upon close examination of video recordings, the sudden movements of iron particles images coincided with light at th

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Abraham, A. Embi Bs MBA. "ENERGY DETECTION IN THE FORM OF LIGHT RADIATION AT END OF HUMAN BLOOD COAGULATION CASCADE- THE OPTICAL ABSORPTION OF WATER VS. FIBRIN BURST ENERGY RELEASE." International Journal of Research - Granthaalayah 7, no. 9 (2019): 200–212. https://doi.org/10.5281/zenodo.3472760.

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The human blood coagulation cascade had been extensively researched from a biochemistry and molecular perspective. The purpose of this manuscript is to introduce a biophysical phenomenon detected via optical microscopy at the end of the human blood coagulation cascade. This could be described as a sudden energy event in the form of light radiation observed once blood tissue movement stops being attracted to metal iron filings or carbon based graphite particles used as sentinels. Upon close examination of video recordings, the sudden movements of iron particles images coincided with light at th

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40

Marinkovic, Sanja Petrusevska, Irena Kondova Topuzovska, Zvonko Milenkovic, and Biserka Kaeva. "The Role of Serum Coagulation Factors in the Differential Diagnosis of Patients with Pneumonia and Parapneumonic Effusion." PRILOZI 37, no. 2-3 (2016): 81–88. http://dx.doi.org/10.1515/prilozi-2016-0020.

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Abstract The aim of this study was to identify the participations of the serum coagulations and fibrinolysis factors that contribute to the differential diagnosis of the patients with community-acquired pneumonia (CAP) without effusion, uncomplicated parapneumonic effusion (UCPPE) and complicated parapneumonic effusion (CPPE). The coagulations system is fundamental for the maintenance of homeostasis, and contributes to the inflammatory process responsible for CAP and the parapneumonic effusion. The factors of coagulations and fibrinolysis participate in the cellular proliferation and migration

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41

Salmanizadeh, H., H. Zolfagharian, and M. Babaie. "Coagulopathy Caused by the Main Anticoagulant Fractions of Echis carinatus Snake Venom on Blood." International Journal of Nano Studies & Technology 4, no. 4 (2015): 93–99. https://doi.org/10.19070/2167-8685-1500018.

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Background: The venom of Viperidae snakes is a compound liquid rich in medicinally active proteins and peptides. It is an invasive weapon for preys immobilization, killing and digestion. Materials and Methods: With a combination of gel and ion exchange chromatography ten sub-fractions were isolated from the E.carinatus venom. Three sub-fractions as anticoagulant sub-fractions were then intravenously injected to mice. Blood sampling was taken before and after injecting these three sub-fractions. The PT, PTT and FT were recorded. Results: Comparison of the PT before and after inje

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42

Maruyama, Ikuro. "Recombinant Thrombomodulin and Activated Protein C in the Treatment of Disseminated Intravascular Coagulation." Thrombosis and Haemostasis 82, no. 08 (1999): 718–21. http://dx.doi.org/10.1055/s-0037-1615902.

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IntroductionThe blood coagulation cascade is regulated by the luminal surface of the endothelial cell lining.1 Endothelial cells synthesize tissue factor pathway inhibitor (TFPI), which, in part, binds to the cell surface glycosaminoglycans and inhibits factors Xa, VIIa, and tissue factor.2 Endothelial cells also produce and exhibit thrombomodulin (TM) on their luminal surface.3 TM is a kind of thrombin receptor that forms a 1:1 complex with thrombin. In this complex, thrombin activates protein C (PC) more than 1,000-fold more than thrombin alone. TM then loses its procoagulant activities, whi

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Starikova, Eleonora A., Jennet T. Mammedova, Artem A. Rubinstein, Alexey V. Sokolov, and Igor V. Kudryavtsev. "Activation of the Coagulation Cascade as a Universal Danger Sign." Current Issues in Molecular Biology 47, no. 2 (2025): 108. https://doi.org/10.3390/cimb47020108.

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Hemostasis is a mechanism that stops bleeding from an injured vessel, involves multiple interlinked steps, culminating in the formation of a “clot” sealing the damaged area. Moreover, it has long been recognized that inflammation also provokes the activation of the coagulation system. However, there has been an increasing amount of evidence revealing the immune function of the hemostasis system. This review collects and analyzes the results of the experimental studies and data from clinical observations confirming the inflammatory function of hemostasis. Here, we summarize the latest knowledge

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Amour, A., J. Hutchinson, A. M. Ruiz Avendaño, et al. "The quest for Factor VIIa exosite inhibitors." Biochemical Society Transactions 35, no. 3 (2007): 555–58. http://dx.doi.org/10.1042/bst0350555.

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Coagulation proteases are involved in a highly orchestrated proteolytic cascade which is essential for haemostasis and blood clotting. In particular, the initiator of the coagulation cascade, Factor VIIa, binds to its cofactor, tissue factor, and its substrate, Factor X, via exosite interactions to form a ternary catalytic complex named extrinsic Xase. These exosite interactions have also been shown to allosterically induce the active conformation of the catalytic site of Factor VIIa. We have developed a direct continuous fluorescence polarization-based extrinsic Xase assay, which has been use

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45

Salman, Tarik, Ahmet Bilici, Cagatay Arslan, et al. "Thrombin activatable fibrinolysis inhibitor, tissue factor pathway inhibitor, and prothrombin fragment 1+2 levels in patients with advanced colorectal cancer." Journal of Clinical Oncology 34, no. 4_suppl (2016): 615. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.615.

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615 Background: Thromboembolism is common in cancer patients.Thrombin activatable fibrinolysis inhibitor (TAFI), tissue factor pathway inhibitor (TFPI) and prothrombin fragment 1+2 (F1+2) are newly identified molecules involved in coagulation and fibrinolysis. The aim of this study was to investigate the relationship between clinicopathologic characteristics and TAFI, TFPI and F1+2 levels in patients with advanced colorectal cancer. Methods: Eighty-two patients (32 metastatic, 50 locally advanced disease) diagnosed with colorectal cancer in the medical oncology clinic, without history of throm

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46

Guerrero-Hurtado, Manuel, Manuel Garcia-Villalba, Alejandro Gonzalo, et al. "Efficient multi-fidelity computation of blood coagulation under flow." PLOS Computational Biology 19, no. 10 (2023): e1011583. http://dx.doi.org/10.1371/journal.pcbi.1011583.

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Clot formation is a crucial process that prevents bleeding, but can lead to severe disorders when imbalanced. This process is regulated by the coagulation cascade, a biochemical network that controls the enzyme thrombin, which converts soluble fibrinogen into the fibrin fibers that constitute clots. Coagulation cascade models are typically complex and involve dozens of partial differential equations (PDEs) representing various chemical species’ transport, reaction kinetics, and diffusion. Solving these PDE systems computationally is challenging, due to their large size and multi-scale nature.

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Ware, Lorraine B., Eric Camerer, Karen Welty-Wolf, Marcus J. Schultz, and Michael A. Matthay. "Bench to bedside: targeting coagulation and fibrinolysis in acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 3 (2006): L307—L311. http://dx.doi.org/10.1152/ajplung.00157.2006.

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Substantial progress has been made in understanding the contribution of alterations in coagulation and fibrinolysis to the pathogenesis of acute lung injury (ALI). Findings from mouse, rat, baboon, and human studies indicate that alterations in coagulation and fibrinolysis may be of major pathogenetic importance in ALI and other inflammatory conditions in the lung including pneumonia, sepsis, and ventilator-induced lung injury. Therapies targeted at both activation of coagulation through the extrinsic coagulation cascade and modulation of coagulation through the protein C system have the poten

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48

Cugno, Massimo, Marco Cicardi, Bianca Bottasso, et al. "Activation of the Coagulation Cascade in C1-Inhibitor Deficiencies." Blood 89, no. 9 (1997): 3213–18. http://dx.doi.org/10.1182/blood.v89.9.3213.

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AbstractActivation of the contact and complement systems in C1-inhibitor deficiencies is thought to contribute to the pathogenesis of angioedema attacks by releasing kinins. Trigger stimuli of attacks may also activate coagulation. This is particularly important because experimental data suggest that thrombin, the main enzyme of the coagulation cascade, increases vascular permeability and can thus influence edema formation. We have studied 19 patients with hereditary angioedema (HAE) during remission, 5 HAE patients during acute attacks, and 6 patients with acquired angioedema (AAE) during rem

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49

HASHIGUCHI, Teruto. "Extrinsic coagulation cascade and diversity of prothrombin time." Japanese Journal of Thrombosis and Hemostasis 27, no. 6 (2016): 631–35. http://dx.doi.org/10.2491/jjsth.27.631.

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Saiah, Eddine, and Chris Soares. "Small Molecule Coagulation Cascade Inhibitors in the Clinic." Current Topics in Medicinal Chemistry 5, no. 16 (2005): 1677–95. http://dx.doi.org/10.2174/156802605775009702.

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