Triggers, targets and treatments for thrombosis

By N. Mackman. Nature, 2008

1,134 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Hematology, Internal Medicine

View Paper: https://www.semanticscholar.org/paper/1908d2299e4be93b76f03fe6c67998cbee402b3e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

In Hematology

In Internal Medicine

Citations in the corpus

Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo (2012, background): “The incidence of VTE increases dramatically over 45 yr of age and ranges from 300,000 to more than two million per year in the United States with similar rates in Europe (Cohen et al., 2007; Heit, 2008; Moll and Mackman, 2008).”
Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo (2009, positive): “Upon vascular injury, platelets rapidly adhere and aggregate to form a plug; simultaneously, coagulation factors respond in a complex reaction cascade to form fibrin, which strengthens platelet clots (Furie and Furie, 2008; Mackman, 2008).”
The pharmacological landscape and therapeutic potential of serine hydrolases (2012, background): “In addition to small-molecule inhibitors, several large biomolecules and their derivatives (proteins, peptides and polysaccharides) that target serine hydrolases, such as thrombin, are either in clinical development or have been approved for clinical us”
Contribution of platelets to tumour metastasis (2011, background): “These agents have many targets, apart from tumour cells (platelets predominantly express prostaglandin G/H synthase 1; also known as COX1”
Endothelial cell control of thrombosis (2015, background): “Similarly, venous thromboembolism can be triggered by disturbed blood flow, hypercoagulable conditions, such as procoagulant changes in the blood, or endothelial activation, and is the major cause of deep vein thrombosis and pulmonary embolism [2, 3].”
Reciprocal coupling of coagulation and innate immunity via neutrophil serine proteases (2010, background): “Our findings show that neutrophil serine proteases, which activate coagulation during systemic infection, also trigger occlusion of large vessels in the absence of a pathogen challenge, resulting in arterial thrombosis, a leading cause of death worldwid”