Evidence for altered hepatic matrix degradation in genetic haemochromatosis

George, D. K.; Ramm, Grant A.; Powell, Lawrie W.; Fletcher, Linda M.; Walker, Neal I.; Cowley, L. L.; Crawford, Darrell H. G.

doi:10.1136/gut.42.5.715

Cited by 22 publications

(11 citation statements)

References 33 publications

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“…(86,87,121,139) Other novel serum-based assessments of fibrosis have also been reported but have yet to be validated in the clinic. (138,140) There is an emerging role for the use of magnetic resonance imaging (MRI) as an accurate, non-invasive measurement of hepatic iron content and the possible detection of fibrosis. There is a high correlation between the mean liver proton transverse relaxation rates measured using MRI and the biochemical liver iron content.…”

Section: Key Developments In Hfe-hhmentioning

confidence: 99%

Hereditary hemochromatosis in the post- HFE era

et al. 2008

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Following the discovery of the HFE gene in 1996 and its linkage to the iron overload disorder hereditary hemochromatosis (HH) there have been profound developments in our understanding of the pathogenesis of the biochemical and clinical manifestations of a number of iron overload disorders. This article provides an update of recent developments and key issues relating to iron homeostasis and inherited disorders of iron overload, with emphasis on HFE-related HH, and is based on the content of the American Association for the Study of Liver Diseases Single-Topic Conference entitled "Hemochromatosis: What has Happened After HFE?" which was held at the Emory

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Section: Key Developments In Hfe-hhmentioning

confidence: 99%

Hereditary hemochromatosis in the post- HFE era

et al. 2008

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“…66 A recent study has demonstrated that patients with hemochromatosis and hepatic fibrosis have increased ratios of TIMP‐1 compared to either collagenase‐1, gelatinase A, or stromelysin‐1. 67 In patients with chronic hepatitis C treated with interferon, responders had an increase in serum collagenase‐1 and a decrease in serum TIMP‐1; nonresponders had the reverse effect, suggesting that interferon may exert a beneficial effect on hepatic fibrosis. 68…”

Section: Serum Mmps and Timps In Liver Diseasementioning

confidence: 99%

Measurement of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Blood and Tissues: Clinical and Experimental Applications

Zucker

Hymowitz

Conner

et al. 1999

Annals of the New York Academy of Sciences

221

130

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The balance between production and activation of MMPs and their inhibition by TIMPs is a crucial aspect of cancer invasion and metastasis. On the basis of the concept that MMPs synthesized in tissues seep into the bloodstream, we have examined MMP levels in the plasma of patients with cancer. In colorectal, breast, prostate, and bladder cancer, most patients with aggressive disease have increased plasma levels of gelatinase B. In patients with advanced colorectal cancer, high levels of either gelatinase B or TIMP complex were associated with shortened survival. We propose that these assays may be clinically useful in characterizing metastatic potential in selected kinds of cancer. In rheumatoid arthritis and systemic lupus erythematosus (SLE), serum and plasma levels of stromelysin-1 were approximately 3-5-fold increased. Fluctuating serum stromelysin-1 levels in SLE did not correspond with change in disease activity. In SLE, stromelysin-1 may be a component of the chronic tissue repair process rather than being responsible for inciting tissue damage. On the basis of these observations, we conclude that measurement of plasma/serum MMP and TIMP levels may provide important data for selecting and following patients considered for treatment with drugs that interfere with MMP activity.

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“…[32][33][34] They showed this to be an iron oxidase located on the basolateral surface of the enterocyte that is required for efficient iron export by ferroportin. 35,36 Grant Ramm focused on ferritin trafficking pathways, 37-39 hepatic stellate cell biology and hepatic fibrosis, [40][41][42] and matrix synthesis and degradation 43,44 and, more recently, on ferritin as a proinflammatory cytokine. 45 Our work on disrupted hepcidin regulation in HFE-associated HH 46 showed, for the first time, that HFE acts as a regulator of hepcidin expression in the liver, rather than being a hepcidin target as previously proposed (Fig.…”

Section: International Influencementioning

confidence: 99%

A career forged in iron

Powell

2014

Hepatology

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Evidence for altered hepatic matrix degradation in genetic haemochromatosis

Cited by 22 publications

References 33 publications

Hereditary hemochromatosis in the post- HFE era

Hereditary hemochromatosis in the post- HFE era

Measurement of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Blood and Tissues: Clinical and Experimental Applications

A career forged in iron

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