Anti‐platelet agents: past, present and future

Cox, Dermot

doi:10.1111/voxs.12529

Cited by 9 publications

(11 citation statements)

References 110 publications

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“…hFcγRIIA‐Tg mice treated with a potent Syk inhibitor 43 do not sustain HIT. Those with engineered IV.3 (to block FcγRIIa ligand binding) do not activate platelets 44 …”

Section: Autoimmune Diseasesmentioning

confidence: 99%

Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis

Patel

Michael

Naik

et al. 2021

Journal of Thrombosis and Haemostasis

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Sepsis and autoimmune diseases remain major causes of morbidity and mortality.The last decade has seen a new appreciation of platelets in host defense, in both immunity and thrombosis. Platelets are first responders in the blood to microbes or non-microbial antigens. The role of platelets in physiologic immunity is counterbalanced by their role in pathology, for example, microvascular thrombosis. Platelets encounter microbes and antigens via both innate and adaptive immune processes; platelets also help to shape the subsequent adaptive response. FcγRIIA is a receptor for immune complexes opsonized by IgG or pentraxins, and expressed in humans by platelets, granulocytes, monocytes and macrophages. With consideration of the roles of IgG and Fc receptors, the host response to microbes and autoantigens can be called adaptive immunothrombosis. Here we review newer developments involving platelet FcγRIIA in humans and humanized mice in immunity and thrombosis, with special attention to heparin-induced thrombocytopenia, systemic lupus erythematosus, and bacterial sepsis. Human genetic diversity in platelet receptors and the utility of humanized mouse models are highlighted.

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“…hFcγRIIA‐Tg mice treated with a potent Syk inhibitor 43 do not sustain HIT. Those with engineered IV.3 (to block FcγRIIa ligand binding) do not activate platelets 44 …”

Section: Autoimmune Diseasesmentioning

confidence: 99%

Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis

Patel

Michael

Naik

et al. 2021

Journal of Thrombosis and Haemostasis

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“…Hence, H6B4-Fab can be further developed. Abciximab, on the other hand, causes long (24–48 h) functional inhibition of GPIIb/IIIa receptors, owing to its high affinity [ 74 , 75 ].…”

Section: Targeting Vwf For the Management Of Co-morbidities In Covid-19 Patientsmentioning

confidence: 99%

Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Choudhary

Sharma

Singh

2021

Chemico-Biological Interactions

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COVID-19 is an ongoing public health emergency that has affected millions of people worldwide and is still a threat to many more. One of the pathophysiological features of COVID-19 is associated with the activation of vascular endothelial cells (ECs) leading to the disruption of vascular integrity, coagulation and inflammation. An interlink mechanism between coagulation and inflammatory pathways has been reported in COVID-19. Multiple components are involved in these pathological pathways. Out of all, Von Willebrand Factor (VWF) is one of the primary components of coagulation pathway and also a mediator of vascular inflammation that plays an important role in thrombo-inflammation that further leads to acute respiratory distress syndrome (ARDS). The thrombo-inflammatory co-morbidities such as hyper-coagulation, thrombosis, ARDS etc. have become the major cause of mortality in the patients of COVID-19 admitted to the ICU. Thus, VWF can be explored as a potential target to manage COVID-19 associated co-morbidities. Supporting this hypothesis, there are literature reports which disclose previous attempts to target VWF for the management of thrombo-inflammation in other pathological conditions. The current report summarizes emerging insights into the pathophysiology, mechanism(s), diagnosis, management and foundations for research on this less explored clinically relevant glycoprotein as coagulation biomarker in COVID-19.

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“…This inhibition is probably not mediated by blocking COX activities or NF- κ B activation but may involve p38 MAPK activity, which plays an essential role in apoptosis activation [ 174 ]. Although the in vitro results are promising, it should be noted that salicylates are known for antiplatelet function, a situation that can be extremely dangerous in the development of severe forms of DENV [ 175 ].…”

Section: Sodium Salicylatementioning

confidence: 99%

Antiviral Role of Phenolic Compounds against Dengue Virus: A Review

et al. 2020

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Phenolic compounds have been related to multiple biological activities, and the antiviral effect of these compounds has been demonstrated in several viral models of public health concern. In this review, we show the antiviral role of phenolic compounds against dengue virus (DENV), the most widespread arbovirus globally that, after its re-emergence, has caused multiple epidemic outbreaks, especially in the last two years. Twenty phenolic compounds with anti-DENV activity are discussed, including the multiple mechanisms of action, such as those directed against viral particles or viral proteins, host proteins or pathways related to the productive replication viral cycle and the spread of the infection.

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Anti‐platelet agents: past, present and future

Cited by 9 publications

References 110 publications

Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis

Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis

Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Antiviral Role of Phenolic Compounds against Dengue Virus: A Review

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