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Articoli di riviste sul tema "Immunothrombose"

Autore: Grafiati

Pubblicato: 16 novembre 2024

Ultima modifica: 31 luglio 2025

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1

Lou, Jianbo, Jianning Zhang, Quanjun Deng, and Xin Chen. "Neutrophil extracellular traps mediate neuro-immunothrombosis." Neural Regeneration Research 19, no. 8 (2023): 1734–40. http://dx.doi.org/10.4103/1673-5374.389625.

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Neutrophil extracellular traps are primarily composed of DNA and histones and are released by neutrophils to promote inflammation and thrombosis when stimulated by various inflammatory reactions. Neutrophil extracellular trap formation occurs through lytic and non-lytic pathways that can be further classified by formation mechanisms. Histones, von Willebrand factor, fibrin, and many other factors participate in the interplay between inflammation and thrombosis. Neuro-immunothrombosis summarizes the intricate interplay between inflammation and thrombosis during neural development and the pathog

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2

Hou, Mengyu, Jingxuan Wu, Jiangshuo Li, et al. "Immunothrombosis: A bibliometric analysis from 2003 to 2023." Medicine 103, no. 37 (2024): e39566. http://dx.doi.org/10.1097/md.0000000000039566.

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Background: Immunothrombosis is a physiological process that constitutes an intravascular innate immune response. Abnormal immunothrombosis can lead to thrombotic disorders. With the outbreak of COVID-19, there is increasing attention to the mechanisms of immunothrombosis and its critical role in thrombotic events, and a growing number of relevant research papers are emerging. This article employs bibliometrics to discuss the current status, hotspots, and trends in research of this field. Methods: Research papers relevant to immunothrombosis published from January 1, 2003, to May 29, 2023, wer

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3

Gashimova, N. R., K. N. Grigoreva, V. O. Bitsadze, et al. "COVID-19, endothelial dysfunction and immunothrombosis." Voprosy ginekologii, akušerstva i perinatologii 23, no. 4 (2024): 47–60. https://doi.org/10.20953/1726-1678-2024-4-47-60.

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SARS-CoV-2 has specific direct and indirect effects on the vascular endothelium, immune system, and hemostasis, thereby promoting endothelial dysfunction, immunothrombosis, and the formation of neutrophil extracellular traps (NETs). In recent years, there has been increasing evidence that endothelial dysfunction, immunothrombosis, and NETosis contribute to the clinical manifestations associated with COVID-19. Endothelial dysfunction is a common denominator of many clinical aspects of severe COVID-19. A better understanding of the pathophysiology of complications may significantly impact patien

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4

Grover, Steven P., and Nigel Mackman. "Neutrophils, NETs, and immunothrombosis." Blood 132, no. 13 (2018): 1360–61. http://dx.doi.org/10.1182/blood-2018-08-868067.

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In this issue of Blood, Yago et al1 describe the mechanism by which neutrophils adhere to activated endothelium and enhance murine venous thrombosis through formation of neutrophil extracellular traps (NETs).

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5

Nappi, Francesco. "Staphylococcus aureus Endocarditis Immunothrombosis." Metabolites 15, no. 5 (2025): 328. https://doi.org/10.3390/metabo15050328.

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Abstract (sommario):

Background: Infective endocarditis continues to represent a challenge for healthcare systems, requiring careful management and resources. Recent studies have indicated a shift in the predominant pathogens of concern, with Streptococcus sp. a being superseded by Staphylococcus sp. and Enterococcus sp. as the leading causes of concern. This shift is of concern as it is associated with Staphylococcus Aureus which has a high virulence rate and a tendency to form a biofilm, meaning that non-surgical therapy may not be effective. It is imperative to deliberate on the likelihood of platelet blood clo

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6

Thakur, Manovriti, Carolina Victoria Cruz Junho, Sarah Maike Bernhard, Marc Schindewolf, Heidi Noels, and Yvonne Döring. "NETs-Induced Thrombosis Impacts on Cardiovascular and Chronic Kidney Disease." Circulation Research 132, no. 8 (2023): 933–49. http://dx.doi.org/10.1161/circresaha.123.321750.

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Abstract (sommario):

Arterial and venous thrombosis constitute a major source of morbidity and mortality worldwide. Association between thrombotic complications and cardiovascular and other chronic inflammatory diseases are well described. Inflammation and subsequent initiation of thrombotic events, termed immunothrombosis, also receive growing attention but are still incompletely understood. Nevertheless, the clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is evident by an increased risk of thrombosis and cardiovascular events in patients with inflammatory or infectious diseas

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7

Chooklin, S., and S. Chuklin. "IMMUNOTHROMBOSIS AS A COMPONENT OF HOST DEFENCE." Fiziolohichnyĭ zhurnal 69, no. 5 (2023): 89–99. http://dx.doi.org/10.15407/fz69.05.089.

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Abstract (sommario):

Immunothrombosis is a normal physiological phenomenon against harmful pathogens that can limit their further spread. It is an important element of the intravascular innate immune system and performs at least four different physiological functions: it helps to capture and localize pathogens; it prevents the invasion of pathogens into tissues by microthrombosis; it contributes to the destruction of pathogens; it helps to recruit additional immune cells to the site of tissue infection and/or damage. The main driving forces of immunothrombosis are platelets, neutrophils and the complement system.

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8

Goshua, George, Ayesha Butt, and Alfred I. Lee. "Immunothrombosis: a COVID‐19 concerto." British Journal of Haematology 194, no. 3 (2021): 491–93. http://dx.doi.org/10.1111/bjh.17666.

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9

Palankar, Raghavendra, and Andreas Greinacher. "Challenging the concept of immunothrombosis." Blood 133, no. 6 (2019): 508–9. http://dx.doi.org/10.1182/blood-2018-11-886267.

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10

Nakazawa, Daigo, and Akihiro Ishizu. "Immunothrombosis in severe COVID-19." EBioMedicine 59 (September 2020): 102942. http://dx.doi.org/10.1016/j.ebiom.2020.102942.

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11

Ebeyer-Masotta, Marie, Tanja Eichhorn, René Weiss, et al. "Heparin-Functionalized Adsorbents Eliminate Central Effectors of Immunothrombosis, including Platelet Factor 4, High-Mobility Group Box 1 Protein and Histones." International Journal of Molecular Sciences 23, no. 3 (2022): 1823. http://dx.doi.org/10.3390/ijms23031823.

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Abstract (sommario):

Inflammation and thrombosis are closely intertwined in numerous disorders, including ischemic events and sepsis, as well as coronavirus disease 2019 (COVID-19). Thrombotic complications are markers of disease severity in both sepsis and COVID-19 and are associated with multiorgan failure and increased mortality. Immunothrombosis is driven by the complement/tissue factor/neutrophil axis, as well as by activated platelets, which can trigger the release of neutrophil extracellular traps (NETs) and release further effectors of immunothrombosis, including platelet factor 4 (PF4/CXCL4) and high-mobi

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12

Aklilu, Addis, Michael Siu-Lun Lai, Zhiwei Jiang, Shea Ping Yip, and Chien-Ling Huang. "Immunothrombosis in Sepsis: Cellular Crosstalk, Molecular Triggers, and Therapeutic Opportunities—A Review." International Journal of Molecular Sciences 26, no. 13 (2025): 6114. https://doi.org/10.3390/ijms26136114.

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Abstract (sommario):

Sepsis remains a critical global health challenge characterized by life-threatening organ dysfunction arising from a dysregulated host response to infection. Immunothrombosis refers to the intersection of immune activation and coagulation pathways, particularly relevant in the context of sepsis. A growing body of evidence identifies immunothrombosis, a tightly interwoven process between innate immunity and coagulation. While immunothrombosis serves as a host defense mechanism under physiological conditions, its aberrant activation in sepsis precipitates microvascular thrombosis, organ ischemia

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13

Ryan, Tristram A. J., Roger J. S. Preston, and Luke A. J. O'Neill. "Immunothrombosis and the molecular control of tissue factor by pyroptosis: prospects for new anticoagulants." Biochemical Journal 479, no. 6 (2022): 731–50. http://dx.doi.org/10.1042/bcj20210522.

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The interplay between innate immunity and coagulation after infection or injury, termed immunothrombosis, is the primary cause of disseminated intravascular coagulation (DIC), a condition that occurs in sepsis. Thrombosis associated with DIC is the leading cause of death worldwide. Interest in immunothrombosis has grown because of COVID-19, the respiratory disease caused by SARS-CoV-2, which has been termed a syndrome of dysregulated immunothrombosis. As the relatively new field of immunothrombosis expands at a rapid pace, the focus of academic and pharmacological research has shifted from gen

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14

Marcos-Jubilar, María, Ramón Lecumberri, and José A. Páramo. "Immunothrombosis: Molecular Aspects and New Therapeutic Perspectives." Journal of Clinical Medicine 12, no. 4 (2023): 1399. http://dx.doi.org/10.3390/jcm12041399.

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Thromboinflammation or immunothrombosis is a concept that explains the existing link between coagulation and inflammatory response present in many situations, such as sepsis, venous thromboembolism, or COVID-19 associated coagulopathy. The purpose of this review is to provide an overview of the current data regarding the mechanisms involved in immunothrombosis in order to understand the new therapeutic strategies focused in reducing thrombotic risk by controlling the inflammation.

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15

Xu, Pengxiang, Liuyan Xin, Xiaoping Xiao, et al. "Neutrophils: As a Key Bridge between Inflammation and Thrombosis." Evidence-Based Complementary and Alternative Medicine 2022 (November 9, 2022): 1–7. http://dx.doi.org/10.1155/2022/1151910.

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Abstract (sommario):

Immunothrombosis is a mechanism of defense of the organism against pathogenic microorganisms that increases their recognition, limitation, and clearance and is part of the innate immune defense. Physiological immunothrombosis is beneficial to the body against the invasion of pathogenic microorganisms, but when immunothrombosis is out of control, it is easy to cause thrombotic diseases, thus, causing unpredictable consequences to the body. Neutrophils play a pivotal role in this process. Understanding the mechanism of neutrophils in immune thrombosis and out-of-control is particularly important

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16

Yost, Christian C. "Pediatric immunothrombosis—Understudied… but what potential!" Pediatric Research 86, no. 1 (2019): 17–18. http://dx.doi.org/10.1038/s41390-019-0389-5.

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17

Páramo, José Antonio, and Ramón Lecumberri. "New mechanisms in venous thrombosis: Immunothrombosis." Medicina Clínica (English Edition) 153, no. 2 (2019): 78–81. http://dx.doi.org/10.1016/j.medcle.2019.05.003.

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18

Hernández-Huerta, María Teresa, Alma Dolores Pérez-Santiago, Laura Pérez-Campos Mayoral, et al. "Mechanisms of Immunothrombosis by SARS-CoV-2." Biomolecules 11, no. 11 (2021): 1550. http://dx.doi.org/10.3390/biom11111550.

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Abstract (sommario):

SARS-CoV-2 contains certain molecules that are related to the presence of immunothrombosis. Here, we review the pathogen and damage-associated molecular patterns. We also study the imbalance of different molecules participating in immunothrombosis, such as tissue factor, factors of the contact system, histones, and the role of cells, such as endothelial cells, platelets, and neutrophil extracellular traps. Regarding the pathogenetic mechanism, we discuss clinical trials, case-control studies, comparative and translational studies, and observational studies of regulatory or inhibitory molecules

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19

Norris, Brandon, Abraham Chorbajian, John Dawi, et al. "Evaluation of Glutathione in Spike Protein of SARS-CoV-2 Induced Immunothrombosis and Cytokine Dysregulation." Antioxidants 13, no. 3 (2024): 271. http://dx.doi.org/10.3390/antiox13030271.

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Thrombotic microangiopathy has been identified as a dominant mechanism for increased mortality and morbidity in coronavirus disease 2019 (COVID-19). In the context of severe COVID-19, patients may develop immunothrombosis within the microvasculature of the lungs, which contributes to the development of acute respiratory distress syndrome (ARDS), a leading cause of death in the disease. Immunothrombosis is thought to be mediated in part by increased levels of cytokines, fibrin clot formation, and oxidative stress. Glutathione (GSH), a well-known antioxidant molecule, may have therapeutic effect

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20

Engelmann, Bernd, and Steffen Massberg. "Innate Immunity, Coagulation, and Thrombosis." Blood 124, no. 21 (2014): SCI—28—SCI—28. http://dx.doi.org/10.1182/blood.v124.21.sci-28.sci-28.

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Abstract In evolutionarily ancient animals such as insects and crustaceans, the host responses to physical injury and to invading pathogens can be mediated by the same mechanism of coagulum formation of the hemolymph. During vertebrate evolution hemostasis has emerged as an independent process primarily involved in the rapid repair of blood vessel injuries. The core processes of hemostasis are blood coagulation (resulting in fibrin formation) and platelet activation. Both processes can independently interact with inflammatory responses as apparent in a pathological context such as during devel

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21

Patel, Pravin, James V. Michael, Ulhas P. Naik та Steven E. McKenzie. "Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis". Journal of Thrombosis and Haemostasis 19, № 5 (2021): 1149–60. http://dx.doi.org/10.1111/jth.15265.

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22

Anitua, Eduardo, Roberto Prado, and Sabino Padilla. "Evolutionary Insight into Immunothrombosis as a Healing Mechanism." International Journal of Molecular Sciences 23, no. 15 (2022): 8346. http://dx.doi.org/10.3390/ijms23158346.

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Both invertebrates and vertebrates possess a cluster of immediate and local wound-sealing, pathogen-killing, and tissue healing responses known as immunoclotting and immunothrombosis, respectively, to cope with two life-threatening emergencies, namely, bleeding and microbial invasion. Despite their convergence in function, immunoclotting and immunothrombosis are deployed by different blood cells and intravascular multidomain proteins. In vertebrates, these proteins share some domains with intrinsic chemical affinities useful in generating cooperative networks such as pathogen and damage patter

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23

Globisch, Maria Ascencion, Favour Chinyere Onyeogaziri, Ross Osborne Smith, Maximiliano Arce, and Peetra Ulrica Magnusson. "Dysregulated Hemostasis and Immunothrombosis in Cerebral Cavernous Malformations." International Journal of Molecular Sciences 23, no. 20 (2022): 12575. http://dx.doi.org/10.3390/ijms232012575.

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Cerebral cavernous malformation (CCM) is a neurovascular disease that affects 0.5% of the general population. For a long time, CCM research focused on genetic mutations, endothelial junctions and proliferation, but recently, transcriptome and proteome studies have revealed that the hemostatic system and neuroinflammation play a crucial role in the development and severity of cavernomas, with some of these publications coming from our group. The aim of this review is to give an overview of the latest molecular insights into the interaction between CCM-deficient endothelial cells with blood comp

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24

Lim, Ming Sheng, and Simon Mcrae. "COVID-19 and immunothrombosis: Pathophysiology and therapeutic implications." Critical Reviews in Oncology/Hematology 168 (December 2021): 103529. http://dx.doi.org/10.1016/j.critrevonc.2021.103529.

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25

Franchi, Thomas, Simon Eaton, Paolo De Coppi, and Stefano Giuliani. "The emerging role of immunothrombosis in paediatric conditions." Pediatric Research 86, no. 1 (2019): 19–27. http://dx.doi.org/10.1038/s41390-019-0343-6.

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26

Jayarangaiah, Apoorva, Pramod Theetha Kariyanna, Xiaoyi Chen, Amog Jayarangaiah, and Abhishek Kumar. "COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response." Clinical and Applied Thrombosis/Hemostasis 26 (January 1, 2020): 107602962094329. http://dx.doi.org/10.1177/1076029620943293.

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Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and

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27

Vazquez-Garza, Eduardo, Carlos Jerjes-Sanchez, Aline Navarrete, Jorge Joya-Harrison, and David Rodriguez. "Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians." Journal of Thrombosis and Thrombolysis 44, no. 3 (2017): 377–85. http://dx.doi.org/10.1007/s11239-017-1528-7.

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28

Eichhorn, Tanja, Silke Huber, René Weiss, et al. "Infection with SARS-CoV-2 Is Associated with Elevated Levels of IP-10, MCP-1, and IL-13 in Sepsis Patients." Diagnostics 13, no. 6 (2023): 1069. http://dx.doi.org/10.3390/diagnostics13061069.

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Immunothrombosis, an excessive inflammatory response with simultaneous overactivation of the coagulation system, is a central pathomechanism in sepsis and COVID-19. It is associated with cellular activation, vascular damage, and microvascular thrombosis, which can lead to multiple organ failure and death. Here, we characterized factors related to immunothrombosis in plasma samples from 78 sepsis patients. In the course of routine clinical testing, SARS-CoV-2 was detected in 14 of these patients. Viral infection was associated with a higher mortality. Both, COVID-19 negative and COVID-19 positi

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29

Slukhanchuk, E. V., V. O. Bitsadze, A. G. Solopova, et al. "Immunothrombosis, tumor progression and metastasis. Role of interleukin-8 and neutrophil extracellular traps." Voprosy ginekologii, akušerstva i perinatologii 22, no. 4 (2023): 48–56. http://dx.doi.org/10.20953/1726-1678-2023-4-48-56.

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Immunothrombosis, tumor progression and metastasis are inextricably linked. These close interactions are carried out by several actors. Neutrophils are considered as players in the antimicrobial host defense. Activated neutrophils release extracellular traps (NETs) involved in antimicrobial immune response and pathogenesis of various conditions including tumor growth. Neutrophils and interleukin-8 (IL-8) play a key role in the formation of NETs. Objective. To evaluate the interaction between NETs and IL-8, their contribution to the development of immunothrombosis and tumor progression in patie

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30

Fakhoury, Hana M. A., Peter R. Kvietys, Ismail Shakir, Hashim Shams, William B. Grant, and Khaled Alkattan. "Lung-Centric Inflammation of COVID-19: Potential Modulation by Vitamin D." Nutrients 13, no. 7 (2021): 2216. http://dx.doi.org/10.3390/nu13072216.

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SARS-CoV-2 infects the respiratory tract and leads to the disease entity, COVID-19. Accordingly, the lungs bear the greatest pathologic burden with the major cause of death being respiratory failure. However, organs remote from the initial site of infection (e.g., kidney, heart) are not spared, particularly in severe and fatal cases. Emerging evidence indicates that an excessive inflammatory response coupled with a diminished antiviral defense is pivotal in the initiation and development of COVID-19. A common finding in autopsy specimens is the presence of thrombi in the lungs as well as remot

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31

Heestermans, Marco, Géraldine Poenou, Anne-Claire Duchez, Hind Hamzeh-Cognasse, Laurent Bertoletti, and Fabrice Cognasse. "Immunothrombosis and the Role of Platelets in Venous Thromboembolic Diseases." International Journal of Molecular Sciences 23, no. 21 (2022): 13176. http://dx.doi.org/10.3390/ijms232113176.

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Venous thromboembolism (VTE) is the third leading cardiovascular cause of death and is conventionally treated with anticoagulants that directly antagonize coagulation. However, recent data have demonstrated that also platelets play a crucial role in VTE pathophysiology. In the current review, we outline how platelets are involved during all stages of experimental venous thrombosis. Platelets mediate initiation of the disease by attaching to the vessel wall upon which they mediate leukocyte recruitment. This process is referred to as immunothrombosis, and within this novel concept inflammatory

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Bautista-Becerril, Brandon, Rebeca Campi-Caballero, Samuel Sevilla-Fuentes, et al. "Immunothrombosis in COVID-19: Implications of Neutrophil Extracellular Traps." Biomolecules 11, no. 5 (2021): 694. http://dx.doi.org/10.3390/biom11050694.

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SARS-CoV-2 is a member of the family of coronaviruses associated with severe outbreaks of respiratory diseases in recent decades and is the causative agent of the COVID-19 pandemic. The recognition by and activation of the innate immune response recruits neutrophils, which, through their different mechanisms of action, form extracellular neutrophil traps, playing a role in infection control and trapping viral, bacterial, and fungal etiological agents. However, in patients with COVID-19, activation at the vascular level, combined with other cells and inflammatory mediators, leads to thrombotic

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Shaw, Rebecca J., Charlotte Bradbury, Simon T. Abrams, Guozheng Wang, and Cheng‐Hock Toh. "COVID‐19 and immunothrombosis: emerging understanding and clinical management." British Journal of Haematology 194, no. 3 (2021): 518–29. http://dx.doi.org/10.1111/bjh.17664.

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Gould, T. J., Z. Lysov, and P. C. Liaw. "Extracellular DNA and histones: double-edged swords in immunothrombosis." Journal of Thrombosis and Haemostasis 13 (June 2015): S82—S91. http://dx.doi.org/10.1111/jth.12977.

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Leppkes, M., A. Lindemann, S. Gößwein, et al. "P075 Neutrophils prevent rectal bleeding in Ulcerative Colitis by peptidyl-arginine deiminase-4-dependent immunothrombosis." Journal of Crohn's and Colitis 16, Supplement_1 (2022): i178—i179. http://dx.doi.org/10.1093/ecco-jcc/jjab232.204.

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Abstract Background Bleeding ulcers and erosions are hallmarks of active ulcerative colitis (UC). However, the mechanisms controlling bleeding and mucosal haemostasis remain elusive. Methods We used high resolution endoscopy and colon tissue samples of active UC (n = 36) as well as experimental models of physical and chemical mucosal damage in mice deficient for peptidyl-arginine deiminase-4 (PAD4), gnotobiotic mice and controls. We employed endoscopy, histochemistry, live-cell microscopy and flow cytometry to study eroded mucosal surfaces during mucosal haemostasis. Results Erosions and ulcer

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Nicolai, Leo, Alexander Leunig, Sophia Brambs, et al. "Immunothrombotic Dysregulation in COVID-19 Pneumonia Is Associated With Respiratory Failure and Coagulopathy." Circulation 142, no. 12 (2020): 1176–89. http://dx.doi.org/10.1161/circulationaha.120.048488.

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Background: Severe acute respiratory syndrome corona virus 2 infection causes severe pneumonia (coronavirus disease 2019 [COVID-19]), but the mechanisms of subsequent respiratory failure and complicating renal and myocardial involvement are poorly understood. In addition, a systemic prothrombotic phenotype has been reported in patients with COVID-19. Methods: A total of 62 subjects were included in our study (n=38 patients with reverse transcriptase polymerase chain reaction–confirmed COVID-19 and n=24 non–COVID-19 controls). We performed histopathologic assessment of autopsy cases, surface ma

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Bokarev, I. N. "Bloodcoagulation. Modern state." Clinical Medicine (Russian Journal) 102, no. 4 (2024): 285–90. http://dx.doi.org/10.30629/0023-2149-2024-102-4-285-290.

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The article provides information on historical issues — the discovery of blood clotting factors, anticoagulant and thrombolytic therapy, on modern understanding, diagnosis and treatment of arterial and venous thrombosis, atherothrombosis, venous thromboembolism, intravascular microthrombosis syndrome, hemophilias and immunothrombosis. Assumptions about the development of atherosclerosis are presented.

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Aarskog, Nikolai Ravn, Ronja Hallem, Jakob Strand Godhavn, and Morten Rostrup. "Time-Dependent Changes in Pulmonary Turnover of Thrombocytes During Critical COVID-19." Critical Care Explorations 6, no. 7 (2024): e1128. http://dx.doi.org/10.1097/cce.0000000000001128.

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OBJECTIVES (BACKGROUND): Under normal conditions, pulmonary megakaryocytes are an important source of circulating thrombocytes, causing thrombocyte counts to be higher in arterial than venous blood. In critical COVID-19, thrombocytes may be removed from the circulation by the lungs because of immunothrombosis, possibly causing venous thrombocyte counts to be higher than arterial thrombocyte counts. In the present study, we investigated time-dependent changes in pulmonary turnover of thrombocytes during critical COVID-19 by measuring arteriovenous thrombocyte differences. We hypothesized that t

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39

Morris, Gerwyn, Chiara C. Bortolasci, Basant K. Puri, et al. "Preventing the development of severe COVID-19 by modifying immunothrombosis." Life Sciences 264 (January 2021): 118617. http://dx.doi.org/10.1016/j.lfs.2020.118617.

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Gaertner, Florian, and Steffen Massberg. "Blood coagulation in immunothrombosis—At the frontline of intravascular immunity." Seminars in Immunology 28, no. 6 (2016): 561–69. http://dx.doi.org/10.1016/j.smim.2016.10.010.

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Bonaventura, Aldo, Alessandra Vecchié, Lorenzo Dagna, et al. "Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19." Nature Reviews Immunology 21, no. 5 (2021): 319–29. http://dx.doi.org/10.1038/s41577-021-00536-9.

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Elliott, Willie, Maheedhara R. Guda, Swapna Asuthkar, et al. "PAD Inhibitors as a Potential Treatment for SARS-CoV-2 Immunothrombosis." Biomedicines 9, no. 12 (2021): 1867. http://dx.doi.org/10.3390/biomedicines9121867.

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Abstract (sommario):

Since the discovery of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, the virus’s dynamicity has resulted in the evolution of various variants, including the delta variant and the more novel mu variant. With a multitude of mutant strains posing as challenges to vaccine efficacy, it is critical that researchers embrace the development of pharmacotherapeutics specific to SARS-CoV-2 pathophysiology. Neutrophil extracellular traps and their constituents, including citrullinated histones, display a linear connection with thrombotic manifestations in COVID-19 patients

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Oliveira, JD, BMM Fonseca, CO Vaz, et al. "TIME COURSE OF THE DEVELOPMENT OF IMMUNOTHROMBOSIS DURING COVID-19 HOSPITALIZATION." Hematology, Transfusion and Cell Therapy 43 (October 2021): S516—S517. http://dx.doi.org/10.1016/j.htct.2021.10.892.

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PAEZ VARGAS, JUAN, ÁNXELA VIDAL GONZáLEZ, DENIS ROBAGLIA, et al. "ANTICOAGULATION, BLEEDING, AND IMMUNOTHROMBOSIS IN CRITICALLY ILL PATIENTS WITH COVID-19." Chest 160, no. 4 (2021): A994—A995. http://dx.doi.org/10.1016/j.chest.2021.07.926.

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Linda, Schönborn, Olga Esteban, Jan Wesche, et al. "Anti-PF4 immunothrombosis without proximate heparin or adenovirus vector vaccine exposure." Blood 142, no. 26 (2023): 2305–14. https://doi.org/10.1182/blood.2023022136.

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46

Helms, Julie, Marine Tschirhart, Anaïs Curtiaud, and Laurent Sattler. "Coagulopathie et sepsis." Médecine Intensive Réanimation, September 5, 2022. http://dx.doi.org/10.37051/mir-00122.

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Abstract (sommario):

La coagulation intravasculaire disséminée (CIVD) est une complication fréquente du sepsis et du choc septique. Alors que l’activation de la coagulation au cours d’un sepsis, conjointement à la mise en jeu de l’immunité innée, participe à la défense de l’hôte contre le pathogène (immunothrombose), son activation dérégulée avec un défaut des systèmes régulateurs anticoagulants et fibrinolytiques dans la CIVD, aboutit à la formation de microthromboses multiples contribuant à la défaillance multiviscérale et à la surmortalité de ces patients. Cette revue de la littérature fait état des dernières a

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Denorme, Frederik, Abigail Ajanel, and Robert A. Campbell. "Immunothrombosis in Neurovascular Disease." Research and Practice in Thrombosis and Haemostasis, December 2023, 102298. http://dx.doi.org/10.1016/j.rpth.2023.102298.

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48

Kvietys, Peter R., Hana M. A. Fakhoury, Sana Kadan, Ahmed Yaqinuddin, Eid Al-Mutairy, and Khaled Al-Kattan. "COVID-19: Lung-Centric Immunothrombosis." Frontiers in Cellular and Infection Microbiology 11 (June 11, 2021). http://dx.doi.org/10.3389/fcimb.2021.679878.

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Abstract (sommario):

The respiratory tract is the major site of infection by SARS-CoV-2, the virus causing COVID-19. The pulmonary infection can lead to acute respiratory distress syndrome (ARDS) and ultimately, death. An excessive innate immune response plays a major role in the development of ARDS in COVID-19 patients. In this scenario, activation of lung epithelia and resident macrophages by the virus results in local cytokine production and recruitment of neutrophils. Activated neutrophils extrude a web of DNA-based cytoplasmic material containing antimicrobials referred to as neutrophil extracellular traps (N

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Wang, Yan, Inge A. Mulder, Willeke F. Westendorp, Jonathan M. Coutinho, and Diederik van de Beek. "Immunothrombosis in Acute Ischemic Stroke." Stroke, October 31, 2024. http://dx.doi.org/10.1161/strokeaha.124.048137.

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Abstract (sommario):

Ischemic stroke is one of the leading causes of disability and mortality worldwide. Thrombosis is the main pathological process of stroke and is therefore an important therapeutic target in stroke prevention. In recent years, with the development of endovascular treatment and therefore retrieving the thrombus for further investigation, evidence is accumulating that immune cells are inextricably linked to stroke pathogenesis. Circulating immune cells have been found to induce immunothrombosis, and they actively participate in the formation of the thrombus by promoting platelet recruitment and t

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Assinger, Alice, Madhumita Chatterjee, and James D. McFadyen. "Editorial: Molecular drivers of immunothrombosis." Frontiers in Immunology 15 (February 27, 2024). http://dx.doi.org/10.3389/fimmu.2024.1385966.

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