Coagulation and anticoagulation in idiopathic pulmonary fibrosis

Crooks, Michael G.; Hart, Simon P.

doi:10.1183/16000617.00008414

Cited by 45 publications

(39 citation statements)

References 52 publications

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“…Unfortunately, this study was terminated early, as warfarin treatment not only failed to show a benefit but was also associated with increased mortality. Although the results of this clinical trial would seem to contradict the hypothesis that coagulation contributes to pulmonary fibrosis, many have since pointed out that the coagulation cascade proteinases have important activities beyond their roles in promoting hemostasis (32,(52)(53)(54). Most notably thrombin, the terminal coagulation proteinase which cleaves fibrinogen to form fibrin, has well-documented signaling activities that can drive downstream proinflammatory and profibrotic pathways (17,22,23,26).…”

Section: Discussionmentioning

confidence: 93%

Uncoupling of the profibrotic and hemostatic effects of thrombin in lung fibrosis

Shea¹,

Probst²,

Brazee³

et al. 2017

JCI Insight

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Section: Discussionmentioning

confidence: 93%

Uncoupling of the profibrotic and hemostatic effects of thrombin in lung fibrosis

Shea¹,

Probst²,

Brazee³

et al. 2017

JCI Insight

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“…Subsequently, a double-blind, randomized, placebo-controlled trial of warfarin was performed, including 145 IPF patients [52]. As opposed to the Kubo study, patients did not receive prednisolone and/or heparin in this particular study, and the study design was also different (lack of blinding and absence of a true placebo-controlled arm in the Kubo study; elegantly reviewed in [53]). In contrast to the Kubo study [50], warfarin did not show a benefit in patients with progressive IPF.…”

Section: Anticoagulant Treatment In Ipfmentioning

confidence: 99%

Targeting coagulation factor receptors – protease‐activated receptors in idiopathic pulmonary fibrosis

Lin

Borensztajn

Spek

2017

Journal of Thrombosis and Haemostasis

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Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with a 5-year mortality rate of > 50% and unknown etiology. Treatment options remain limited and, currently, only two drugs are available, i.e. nintedanib and pirfenidone. However, both of these antifibrotic agents only slow down the progression of the disease, and do not remarkably prolong the survival of IPF patients. Hence, the discovery of new therapeutic targets for IPF is crucial. Studies exploring the mechanisms that are involved in IPF have identified several possible targets for therapeutic interventions. Among these, blood coagulation factor receptors, i.e. protease-activated receptors (PARs), are key candidates, as these receptors mediate the cellular effects of coagulation factors and play central roles in influencing inflammatory and fibrotic responses. In this review, we will focus on the controversial role of the coagulation cascade in the pathogenesis of IPF. In the light of novel data, we will attempt to reconciliate the apparently conflicting data and discuss the possibility of pharmacologic targeting of PARs for the treatment of fibroproliferative diseases.

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“…A link between blood coagulation and pulmonary fibrosis is well recognised [91]. Based on the role of microparticles in blood coagulation, we investigated their presence in diffuse parenchymal lung disease patients [49].…”

Section: Diffuse Parenchymal Lung Diseasesmentioning

confidence: 99%

Cell-derived microparticles and the lung

et al. 2016

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Cell-derived microparticles are small (0.1-1 μm) vesicles shed by most eukaryotic cells upon activation or during apoptosis. Microparticles carry on their surface, and enclose within their cytoplasm, molecules derived from the parental cell, including proteins, DNA, RNA, microRNA and phospholipids. Microparticles are now considered functional units that represent a disseminated storage pool of bioactive effectors and participate both in the maintenance of homeostasis and in the pathogenesis of diseases. The mechanisms involved in microparticle generation include intracellular calcium mobilisation, cytoskeleton rearrangement, kinase phosphorylation and activation of the nuclear factor-κB. The role of microparticles in blood coagulation and inflammation, including airway inflammation, is well established in in vitro and animal models. The role of microparticles in human pulmonary diseases, both as pathogenic determinants and biomarkers, is being actively investigated. Microparticles of endothelial origin, suggestive of apoptosis, have been demonstrated in the peripheral blood of patients with emphysema, lending support to the hypothesis that endothelial dysfunction and apoptosis are involved in the pathogenesis of the disease and represent a link with cardiovascular comorbidities. Microparticles also have potential roles in patients with asthma, diffuse parenchymal lung disease, thromboembolism, lung cancer and pulmonary arterial hypertension. @ERSpublications Microparticles are potential biomarkers and targets for therapeutic interventions in respiratory medicine http://ow.ly/ZTCp6

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Coagulation and anticoagulation in idiopathic pulmonary fibrosis

Cited by 45 publications

References 52 publications

Uncoupling of the profibrotic and hemostatic effects of thrombin in lung fibrosis

Uncoupling of the profibrotic and hemostatic effects of thrombin in lung fibrosis

Targeting coagulation factor receptors – protease‐activated receptors in idiopathic pulmonary fibrosis

Cell-derived microparticles and the lung

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