Current Perspectives in the Antiplatelet Therapy of Thrombotic Disorders

Hk, Breddin

doi:10.1055/s-2007-1002697

Cited by 2 publications

(2 citation statements)

References 15 publications

(17 reference statements)

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“…PTF may act as a potential antifibrogenic agent by inhibiting cell proliferation and/or collagen deposition in cell types responsible for the accumulation of extracellular matrix 32. Romanelli et al 33 suggested that the antifibrogenic action of PTF on human HSCs is mainly mediated by extracellular collagen degradation rather than by a reduction of collagen synthesis.…”

Section: Potential Anticoagulant Treatment Strategies Affecting Fibrosismentioning

confidence: 99%

Coagulation and fibrosis in chronic liver disease

Calvaruso

Maimone

Gatt

et al. 2008

Gut

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In the hepatic tissue repair mechanism, hepatic stellate cells (HSCs) are recruited at the site of injury and their changes reflect paracrine stimulation by all neighbouring cell types, including sinusoidal endothelial cells, Kupffer cells, hepatocytes, platelets and leucocytes. Thrombin converts circulating fibrinogen to fibrin, promotes platelet aggregation, is a potent activator of endothelial cells, acts as a chemoattractant for inflammatory cells and is a mitogen and chemoattractant for fibroblasts and vascular smooth muscle cells. Most of the cellular effects elicited by thrombin are mediated via a family of widely expressed G-protein-coupled receptors termed protease activated receptors (PARs). All known members of the PAR family stimulate cell proliferation/activation in a rat HSC line. Thrombin receptors are constitutively expressed in the liver, and their expression increases in parallel with the severity and/or the duration of liver disease. In human studies, thrombotic risk factors were found to be independently associated with the extent of fibrosis; severity of hepatitis C virus (HCV)-associated liver disease appears to be less in patients with haemophilia when compared with those with HCV alone. Several studies, based mostly on rat models, demonstrate that anticoagulants or antiplatelet agents prevent hepatic necrosis and fibrosis by acting on HSCs. These drugs could be therapeutic agents in patients with chronic liver disease and specific studies should be initiated.

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Section: Potential Anticoagulant Treatment Strategies Affecting Fibrosismentioning

confidence: 99%

Coagulation and fibrosis in chronic liver disease

Calvaruso

Maimone

Gatt

et al. 2008

Gut

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“…These include factors emanating from various parenchymal cells, lar properties to those of dipyridamole. Pentoxifylline increases plasma adenosine, inhibits platelet aggregation, 61 inlymphocytes, macrophages, and platelets. One of the most potent of these factors is the platelet-derived growth factor.…”

Section: Aid Hepa 0023mentioning

confidence: 99%

Hepatic sinusoidal fibrosis induced by cholesterol and stilbestrol in the rabbit: 1. Morphology and inhibition of fibrogenesis by dipyridamole

1996

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tween individual animals. It has been shown that rabbits This study documents the hepatic morphology and the that are given CHOL simultaneously with diethylstilbestrol ultrastructure of a model of hepatic fibrosis in rabbits.(DES) rapidly develop hepatic fibrosis over a period of several Rabbits were given a cholesterol-supplemented diet weeks, 6-8 but this model has not been studied in detail. The (1%), a stilbestrol diet (10 mg subcutaneously twice a present report describes the hepatic morphology, the ultraweek), or both treatments simultaneously for 7 weeks.structure, and the hepatic collagen content following this Rabbits given the combined treatment developed sinu- The treatments were given for 7 weeks, at which point the animals were killed. One D-C rabbit died before the completion of the study. Hepatic fibrosis develops in a variety of mammals that areThe liver and spleen were exposed under sodium pentobarbital anesfed a cholesterol (CHOL)-supplemented diet.1-5 However, in thesia without prior fasting, and samples were excised, diced, and most species, including the rabbit, the fibrosis is mild, re-fixed by immersion in cold 2.5% glutaraldehyde buffered with 0.1 quires many months to develop, and is highly variable be-mol/L of cacodylate at pH 7.2. This tissue was later postfixed with osmium tetroxide, embedded in Epon 812, and the sections were stained with lead citrate and uranyl acetate. The spleens were cut Abbreviations: CHOL, cholesterol; D-C, diethylstilbestrol-cholesterol; DES, diethylstilinto 5-mm slices and allowed to drain on absorbent paper before bestrol.weighing. The liver slices were fixed in buffered 4% formaldehyde,

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Current Perspectives in the Antiplatelet Therapy of Thrombotic Disorders

Cited by 2 publications

References 15 publications

Coagulation and fibrosis in chronic liver disease

Coagulation and fibrosis in chronic liver disease

Hepatic sinusoidal fibrosis induced by cholesterol and stilbestrol in the rabbit: 1. Morphology and inhibition of fibrogenesis by dipyridamole

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