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      간섬유화 = Review : Hepatic Fibrogenesis

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      https://www.riss.kr/link?id=A75372475

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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      In acute injury, liver recovers completely without any scarring change or complication. However, large portion of liver is changed into fibrotic state by excessive production of extracellular matrix (ECM) under chronic injury. Excessive production of ECM results in hepatic fibrosis and repeated process of hepatic fibrosis progress into liver cirrhosis. Liver cirrhosis is an irreversible and terminal state of chronic liver disease and one of the major causes of death in Korea. To block the progression to liver cirrhosis, various studies in the field of virology and immunology have been proceeded. Recently, studies on the hepatic fibrogenesis have progressed with the development of molecular biology. Hepatic stellate cells (HSC) play a key role in the pathogenesis of hepatic fibrosis by producing ECM. The degree of hepatic fibrosis depends on the proliferation and activation of HSC and increased net production of collagen. Therefore, inhibition of HSC activation is one of the main ways to block the progression of hepatic fibrosis. Many kinds of factors such as oxidative stress, acetaldehyde, ascorbic acid, transforming growth factor-beta (TGF-β) and carbon tetrachloride (CCl4) have been reported to activate HSC and stimulate collagen gene expression. Although there are no definite and effective antifibrogenic agents, possible candidates are antioxidants, interferon, retinoids such as β-carotene, flavonoids, renin-angiotensin system inhibitors and peroxisome proliferator activated receptor-gamma (PPAR-gamma) agonists. We tried to evaluate the characteristics of HSC in order to develop agents that inhibit hepatic fibrogenesis. (Korean J Gastroenterol 2006;48:297-305)
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      In acute injury, liver recovers completely without any scarring change or complication. However, large portion of liver is changed into fibrotic state by excessive production of extracellular matrix (ECM) under chronic injury. Excessive production of ...

      In acute injury, liver recovers completely without any scarring change or complication. However, large portion of liver is changed into fibrotic state by excessive production of extracellular matrix (ECM) under chronic injury. Excessive production of ECM results in hepatic fibrosis and repeated process of hepatic fibrosis progress into liver cirrhosis. Liver cirrhosis is an irreversible and terminal state of chronic liver disease and one of the major causes of death in Korea. To block the progression to liver cirrhosis, various studies in the field of virology and immunology have been proceeded. Recently, studies on the hepatic fibrogenesis have progressed with the development of molecular biology. Hepatic stellate cells (HSC) play a key role in the pathogenesis of hepatic fibrosis by producing ECM. The degree of hepatic fibrosis depends on the proliferation and activation of HSC and increased net production of collagen. Therefore, inhibition of HSC activation is one of the main ways to block the progression of hepatic fibrosis. Many kinds of factors such as oxidative stress, acetaldehyde, ascorbic acid, transforming growth factor-beta (TGF-β) and carbon tetrachloride (CCl4) have been reported to activate HSC and stimulate collagen gene expression. Although there are no definite and effective antifibrogenic agents, possible candidates are antioxidants, interferon, retinoids such as β-carotene, flavonoids, renin-angiotensin system inhibitors and peroxisome proliferator activated receptor-gamma (PPAR-gamma) agonists. We tried to evaluate the characteristics of HSC in order to develop agents that inhibit hepatic fibrogenesis. (Korean J Gastroenterol 2006;48:297-305)

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      참고문헌 (Reference)

      1 "perisinusoidal cells with special reference to storage of vitamin A" 429-462, amjanat1971

      2 "d-α-Tocopherol inhibits collagen α1(I)gene expression in cultured human fibroblast" 87 : 2230-2235, 1991

      3 "a target enzyme for drug development design of suppressive agents and the in vitro effects of inhibitors and proinhibitors" 3 8-16, jhepatol1991

      4 "Tumor necrosis factor α inhibits collagen gene transcription and collagen synthesis in cultured human fibroblast" 263 : 5841-5845, 1988

      5 "Transforming growth factor β1 and α in chronic liver disease:Effect of interferon alfa therapy" 324 : 933-940, 1991

      6 "Therapeutic strategies of hepatic fibrosis" 8 : 176-182, 1988

      7 "The crosslinking of the collagen and elastin:enzymatic conversion of lysine in peptide linkage to alleysine by an extract from bone" 61 : 708-714, 1968

      8 "The cellular basis of hepatic fibrosis" 328 : 1828-1835, 1993

      9 "TGF β and collagen α1(I)gene expression are increased in hepatic acinar zone 1 of rat with iron overload" 267 : 1994

      10 "Synthesis of cellular fibronectin by rat liver fat storing cells:regulation by cytokines" 103 : 1313-1321, 1992

      1 "perisinusoidal cells with special reference to storage of vitamin A" 429-462, amjanat1971

      2 "d-α-Tocopherol inhibits collagen α1(I)gene expression in cultured human fibroblast" 87 : 2230-2235, 1991

      3 "a target enzyme for drug development design of suppressive agents and the in vitro effects of inhibitors and proinhibitors" 3 8-16, jhepatol1991

      4 "Tumor necrosis factor α inhibits collagen gene transcription and collagen synthesis in cultured human fibroblast" 263 : 5841-5845, 1988

      5 "Transforming growth factor β1 and α in chronic liver disease:Effect of interferon alfa therapy" 324 : 933-940, 1991

      6 "Therapeutic strategies of hepatic fibrosis" 8 : 176-182, 1988

      7 "The crosslinking of the collagen and elastin:enzymatic conversion of lysine in peptide linkage to alleysine by an extract from bone" 61 : 708-714, 1968

      8 "The cellular basis of hepatic fibrosis" 328 : 1828-1835, 1993

      9 "TGF β and collagen α1(I)gene expression are increased in hepatic acinar zone 1 of rat with iron overload" 267 : 1994

      10 "Synthesis of cellular fibronectin by rat liver fat storing cells:regulation by cytokines" 103 : 1313-1321, 1992

      11 "Structure of the extracellular matrix in normal and fibrotic liver:collagens and glycoproteins" 10 : 1-10, 1990

      12 "Stimulation of collagen α1 gene expression is associated with lipid peroxidation in hepatocellular injury a link to tissue fibrosis" Trautwein C 1262-1271, hepatology1994

      13 "Retinol release by activated rat hepatic lipocytes:regulation by Kupffer cell conditioned medium and PDGF" 264 : 1993

      14 "Retinoic acid suppresses the response to PDGF in human hepatic Ito cell like myofibroblasts" 294 : 785-791, 1993

      15 "Pentoxifylline blocks hepatic stellate cell activation independently of phosphodiesterase inhibitory activity" 273 : 1094-1100, 1997

      16 "Oxidative stress effect on the activation of hepatic stellate cells" 42 : 1-8, 2001

      17 "New perspectives in cell adhesion:RGD and integrin" 238 : 491-497, 1987

      18 "Molecular dissection of the mitogenic effect of hepatocytes on cultured hepatic stellate cells" 22 : 1507-1518, 1995

      19 "Long- and short-term D-alpha-tocopherol supplementation inhibits liver collagen alpha1 (I) gene expression" 275 : 1480-1485, 1998

      20 "Immunolocalization of laminin in normal rat liver and biosynthesis of laminin by hepatic lipocytes in primary culture" 94 : 1053-1062, 1988

      21 "Identification and partial characterization of a hepatocyte derived factor promoting proliferation of cultured fat storing cells" 16 : 1250-1266, 1992

      22 "Hepatocyte collagen production in vivo in normal rats" 78 : 333-339, 1986

      23 "Hepatic lipocytes.the principal collagen producing cells of normal rat liver" 82 : 8681-8685, 1985

      24 "Electron immunohistochemical studies in rats with CCl4 induced cirrhosis" 166-186,

      25 "Effect of PDGF and other polypeptide mitogens on DNA synthesis and growth of cultured rat liver fat storing cells" 84 : 1786-1793, 1989

      26 "Differential effect of interleukin 1 alpha,tumor necrosis alpha,and transforming growth factor beta 1 on cell proliferation and collagen formation by cultured fat storing cells" 9 : 71-78, 1989

      27 "Collagen types in normal and cirrhotic liver" 76 : 710-719, 1979

      28 "Collagen production in fat storing cells after CCl4 intoxication in the rat:immunoelectron microscopic observation of type I,type III collagens,and prolyl hydroxylase" 59 : 509-521, 1988

      29 "Cellular sources of noncollagenous matrix proteins:role of fat storing cells in fibrogenesis" 10 : 30-46, 1990

      30 "Cell matrix interaction and hepatic fibrosis" 9 : 143-155, 1990

      31 "Apoptosis of hepatic stellate cells in CCl4 induced acute liver injury of the rat" 39 : 960-966, 2003

      32 "Alternative splicing products of the tenascin gene distinguish rat liver fat storing cells from arterial smooth muscle cells and skin fibroblasts" 16 : 768-775, 1992

      33 "Activation of rat liver perisinusoidal lipocytes by transforming growth factors derived from myofibroblast like cells:a poten-tial mechanism of self perpetuation in liver fibrogenesis" 89 : 19-27, 1992

      34 "Activation of hepatic stellate cells by TGF α and collagen type I is mediated by oxidative stress through c-myb expression" 96 : 2461-2468, 1995

      35 "A subunit model for the tropocollagen macromolecule" 51 : 871-876, 1964

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2022 평가예정 재인증평가 신청대상 (재인증)
      2019-01-01 평가 등재학술지 유지 (계속평가) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2002-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      1999-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.18 0.18 0.18
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.21 0.2 0.315 0.03
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