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• W1509809343 abstract "Liver diseases occur quite frequently in dogs; the overall incidence in dogs has been estimated around 1-2% of the clinical cases. Most liver diseases are, like in humans, chronic and occur through chronic inflammation due to different causes. In all cases the on-going liver cell damage leads to a reduction of the functional liver cell mass and progressive deposition of fibrous tissue in the liver. These two phenomena, atrophy and fibrosis, are two sides of one medal and go hand in hand to cause fatal liver dysfunction in the end stage. The large regenerative capacity of the liver is lost in the course of chronic disease. There is convincing evidence that the two main counteracting factors, Hepatocyte Growth Factor (HGF) and Transforming Growth Factor-β1 (TGF-β1), determine the outcome of liver disease. HGF is the principal factor stimulating the liver to grow and regenerate and suppresses fibrosis and apoptosis. In contrast, TGF-β1 induces formation of excessive fibrous tissue and a reduction of the regenerative capacity together with stimulation of cell death. The findings with respect to the crucial counteracting effects of HGF and TGF-β1 in liver growth, regeneration and fibrosis, have stimulated researchers to investigate the potential of administering HGF to experimental animals given hepatotoxic or fibrogenic drugs. Administration of HGF completely prevented or, when given afterwards, reversed toxic effects. Even in cases of chronic damage with already formed disruption of the normal micro-architecture of the liver, fibrosis and atrophy (cirrhosis), this phenomenon could largely be reversed. Furthermore, the normal fatal course of peracute fulminant hepatitis (severe acute hepatic sepsis or toxicity) could be prevented in experimental animals. The few studies in dogs indicate that the above findings also apply to this species. Interestingly, one of the first reports of a very potent liver regeneration stimulating factor (now known as HGF) was found in dogs. Extrapolation for the above mentioned rodent models to human medicine has not been achieved. The use of novel therapeutic approaches in dogs presented at the veterinary clinic could be seen as a much more relevant animal model for the translation to human clinical medicine. For instance, HGF treatment during normally life-threatening hepatic diseases could cause a revolution in the treatment of liver diseases (in both man and dog). Therapeutic intervention could be achieved by the addition of the HGF-glycoprotein itself. Alternatively, and in line with the concept that the clinical outcome is determined by the balance between HGF and TGF-β1, gene therapy approaches resulting in blocking the effects of TGF-β1 have been similarly effective, at least in chronic disease models. Taken together, the central theme of this thesis involves several aims. The first aim is to describe the regulatory roles of Hepatocyte Growth Factor (HGF) and Transforming Growth Factor-β1 (TGF-β1), via the respective receptors c-MET and TGF-β1 receptors type II and I in growth, regeneration, and formation of fibrosis in a variety of liver diseases. Second, development of therapeutic tools based on the above insights to treat liver diseases characterized by inadequate growth or atrophy with fibrosis and/or cirrhosis, especially by influencing the balance between HGF and TGF-β1 in the liver. Finally, initial evaluation of the effects of such therapeutic tools." @default.
• W1509809343 created "2016-06-24" @default.
• W1509809343 creator A5006972265 @default.
• W1509809343 date "2006-04-06" @default.
• W1509809343 modified "2023-09-27" @default.
• W1509809343 title "Regenerative and fibrotic pathways in canine liver disease" @default.
• W1509809343 cites W1212464357 @default.
• W1509809343 cites W132936908 @default.
• W1509809343 cites W1482629448 @default.
• W1509809343 cites W1488035356 @default.
• W1509809343 cites W1515573227 @default.
• W1509809343 cites W1521417371 @default.
• W1509809343 cites W1528606854 @default.
• W1509809343 cites W1536476892 @default.
• W1509809343 cites W1557686543 @default.
• W1509809343 cites W1565561072 @default.
• W1509809343 cites W1566771372 @default.
• W1509809343 cites W1572735583 @default.
• W1509809343 cites W1577577364 @default.
• W1509809343 cites W1592550864 @default.
• W1509809343 cites W1597914794 @default.
• W1509809343 cites W1598516408 @default.
• W1509809343 cites W1605709431 @default.
• W1509809343 cites W1611419331 @default.
• W1509809343 cites W1636022999 @default.
• W1509809343 cites W163630733 @default.
• W1509809343 cites W1649526546 @default.
• W1509809343 cites W1745634660 @default.
• W1509809343 cites W1791888878 @default.
• W1509809343 cites W1823530219 @default.
• W1509809343 cites W1840163537 @default.
• W1509809343 cites W184311987 @default.
• W1509809343 cites W1920968130 @default.
• W1509809343 cites W1923651867 @default.
• W1509809343 cites W1932132006 @default.
• W1509809343 cites W1933984510 @default.
• W1509809343 cites W193903826 @default.
• W1509809343 cites W1945294208 @default.
• W1509809343 cites W1964073353 @default.
• W1509809343 cites W1965202020 @default.
• W1509809343 cites W1965206203 @default.
• W1509809343 cites W1966543080 @default.
• W1509809343 cites W1968921354 @default.
• W1509809343 cites W1969732147 @default.
• W1509809343 cites W1971741728 @default.
• W1509809343 cites W1972144299 @default.
• W1509809343 cites W1972239225 @default.
• W1509809343 cites W1974364517 @default.
• W1509809343 cites W1975710755 @default.
• W1509809343 cites W1975835742 @default.
• W1509809343 cites W1975898748 @default.
• W1509809343 cites W1976752592 @default.
• W1509809343 cites W1977695060 @default.
• W1509809343 cites W1978116541 @default.
• W1509809343 cites W1978232265 @default.
• W1509809343 cites W1978857300 @default.
• W1509809343 cites W1980055557 @default.
• W1509809343 cites W1980755015 @default.
• W1509809343 cites W1982099849 @default.
• W1509809343 cites W1983086656 @default.
• W1509809343 cites W1984769959 @default.
• W1509809343 cites W1989998925 @default.
• W1509809343 cites W1990332775 @default.
• W1509809343 cites W1990378084 @default.
• W1509809343 cites W1991386830 @default.
• W1509809343 cites W1991863158 @default.
• W1509809343 cites W1992844265 @default.
• W1509809343 cites W1993034428 @default.
• W1509809343 cites W1993605018 @default.
• W1509809343 cites W1994738588 @default.
• W1509809343 cites W1995137799 @default.
• W1509809343 cites W1995191901 @default.
• W1509809343 cites W1996389318 @default.
• W1509809343 cites W1996446862 @default.
• W1509809343 cites W1997928934 @default.
• W1509809343 cites W1998316074 @default.
• W1509809343 cites W1998420703 @default.
• W1509809343 cites W1998453356 @default.
• W1509809343 cites W1998932597 @default.
• W1509809343 cites W1999253766 @default.
• W1509809343 cites W2000935132 @default.
• W1509809343 cites W2002023508 @default.
• W1509809343 cites W2002469066 @default.
• W1509809343 cites W2003089081 @default.
• W1509809343 cites W2003300606 @default.
• W1509809343 cites W2003742649 @default.
• W1509809343 cites W2004121042 @default.
• W1509809343 cites W2004471846 @default.
• W1509809343 cites W2005782838 @default.
• W1509809343 cites W2006077720 @default.
• W1509809343 cites W2006773200 @default.
• W1509809343 cites W2007064404 @default.
• W1509809343 cites W2007733439 @default.
• W1509809343 cites W2008399598 @default.
• W1509809343 cites W2008546766 @default.
• W1509809343 cites W2009655979 @default.
• W1509809343 cites W2009745570 @default.
• W1509809343 cites W2010081774 @default.
• W1509809343 cites W2010846405 @default.
• W1509809343 cites W2014484446 @default.

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