المؤلفون: Lopez-Posadas, R, Fastancz, P, Martinez-Sanchez, LD, Panteleev-Ivlev, J, Thonn, V, Kisseleva, T, Becker, LS, Schulz-Kuhnt, A, Zundler, S, Wirtz, S, Atreya, R, Carle, B, Friedrich, O, Schurmann, S, Waldner, MJ, Neufert, C, Brakebusch, CH, Bergo, MO, Neurath, MF, Atreya, I

المصدر: Gastroenterology. 157(5):1293-1309

مصطلحات موضوعية: Medicin och hälsovetenskap

URL الوصول: http://kipublications.ki.se/Default.aspx?queryparsed=id:142146989

المؤلفون: Llorente, C, Jepsen, P, Inamine, T, Wang, L, Bluemel, S, Wang, HJ, Loomba, R, Bajaj, JS, Schubert, ML, Sikaroodi, M, Gillevet, PM, Xu, J, Kisseleva, T, Ho, SB, Depew, J, Du, X, Sørensen, HT, Vilstrup, H, Nelson, KE, Brenner, DA, Fouts, DE, Schnabl, B

المصدر: Nature Communications. 8(1)

الوصف: Chronic liver disease is rising in western countries and liver cirrhosis is the 12th leading cause of death worldwide. Simultaneously, use of gastric acid suppressive medications is increasing. Here, we show that proton pump inhibitors promote progression of alcoholic liver disease, non-alcoholic fatty liver disease, and non-alcoholic steatohepatitis in mice by increasing numbers of intestinal Enterococcus spp. Translocating enterococci lead to hepatic inflammation and hepatocyte death. Expansion of intestinal Enterococcus faecalis is sufficient to exacerbate ethanol-induced liver disease in mice. Proton pump inhibitor use increases the risk of developing alcoholic liver disease among alcohol-dependent patients. Reduction of gastric acid secretion therefore appears to promote overgrowth of intestinal Enterococcus, which promotes liver disease, based on data from mouse models and humans. Recent increases in the use of gastric acid-suppressive medications might contribute to the increasing incidence of chronic liver disease.

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URL الوصول: https://escholarship.org/uc/item/52b7r3gz

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المؤلفون: Kisseleva, T. P.^Aff3, Bobylev, V. V.^Aff3, Bronnikova, N. M.^Aff3, Dementjeva, A. A.^Aff3, Kalinichenko, O. A.^Aff3, Kisselev, A. A.^Aff3, Potter, H. I.^Aff3, Tolbin, S. V.^Aff3, Shakht, N. A.^Aff3

المساهمون: Lieske, Jay H., editor^Aff1, Abalakin, Victor K., editor^Aff2

المصدر: Inertial Coordinate System on the Sky : Proceedings of the 141st Symposium of the International Astronomical Union Held in Leningrad, U.S.S.R., October 17–21, 1989. 141:73-74

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المؤلفون: Xu J, Liu X, Brenner DA, Kisseleva T

المصدر: Cell Health and Cytoskeleton, Vol 2015, Iss default, Pp 111-119 (2015)

مصطلحات موضوعية: lcsh:R5-920, lcsh:Medicine (General)

الوصف: Jun Xu,1,2 Xiao Liu,1,2 David A Brenner,1 Tatiana Kisseleva2 1Department of Medicine, 2Department of Surgery, University of California, San Diego, CA, USA Abstract: Liver fibrosis results from chronic liver injury that causes hepatocellular damage. Damaged hepatocytes apoptose, and release factors that facilitate recruitment of leukocytes to the site of injury, which in turn mediate recruitment and activation of liver- resident (Kupffer cells) and bone marrow (BM)-derived macrophages. Activated macrophages secrete TGF-ß1, the major profibrogenic cytokine, which activates hepatic myofibroblasts, which are not present in the liver under physiological conditions. Several sources of myofibroblasts have been identified, but it is believed that liver-resident hepatic stellate cells (HSCs) and portal fibroblasts (PFs) are the major source of hepatic myofibroblasts in fibrotic liver. Fibrocytes, designated as BM-derived collagen Type I producing cells, were also implicated in liver fibrosis; hence, their contribution to liver fibrosis remains controversial. Upon removal of the etiological agent, myofibroblasts either undergo apoptosis or inactivate into a quiescent-like state, followed by resorbtion of the fibrous scar. However, prolonged/repeated liver injury triggers irreversible cross-linking of collagen fibers that prevents fibrous scar from collagenase-mediated degradation. This review will discuss several types of fibrogenic cells contributing to the myofibroblast population, and the signaling pathways regulating their activation and collagen deposition. Keywords: Liver fibrosis, TGF-ß1 signaling, hepatic stellate cells, portal fibroblasts, fibrocytes, collagen Type I deposition

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doajarticles::a2e70dba745e66abb725d6b636507597
http://www.dovepress.com/novel-perspectives-on-the-origins-of-the-hepatic-myofibroblasts-peer-reviewed-article-CHC