[1] Werner H, Jr RC, Leroith D. The regulation of IGF-I receptor gene expression by positive and negative zinc-finger transcription factors. Adv Exp Med Biol, 1993, 343: 91-103.
[2] Bataller R, Brenner DA. Liver fibrosis. J Clin Invest, 2005, 115: 209.
[3] Bataller R, Brenner DA. Liver fibrosis. J Clin Invest, 2005, 115: 1100.
[4] Elpek GÖ. Cellular and molecular mechanisms in the pathogenesis of liver fibrosis: An update. World J Gastroenterol, 2014, 20: 7260-7276.
[5] Lara-Diaz VJ,Castilla-Cortazar I,Martin-Estal I,et al.IGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture.J Physiol Biochem,2017, 73: 245-258.
[6] Tutau F, Rodríguezortigosa C, Puche JE, et al. Enhanced actions of insulin-like growth factor-I and interferon-alpha co-administration in experimental cirrhosis. Liver Int,2009, 29: 37-46.
[7] Hao CN, Geng YJ, Li F, et al. Insulin-like growth factor-1 receptor activation prevents hydrogen peroxide-induced oxidative stress, mitochondrial dysfunction and apoptosis. Apoptosis, 2011, 16: 1118-1127.
[8] Pérez R, García-Fernández M, Díaz-Sánchez M, et al. Mitochondrial protection by low doses of insulin-like growth factor-Iin experimental cirrhosis. World J Gastroenterol, 2008, 14: 2731-2739.
[9] 叶晓光, 廖云珍, 黄远明,等. 胰岛素样生长因子Ⅰ和各型肝病关系的研究. 临床肝胆病杂志, 2002, 18: 37-38.
[10] Donaghy A, Ross R, Gimson A, et al. Growth hormone, insulinlike growth factor-1, and insulinlike growth factor binding proteins 1 and 3 in chronic liver disease.. Hepatology, 1995, 21: 680-688.
[11] Cuneo RC, Hickman PE, Wallace JD, et al. Altered endogenous growth hormone secretory kinetics and diurnal GH-binding protein profiles in adults with chronic liver disease.Clin Endocrinol (Oxf), 1995, 43: 265-275.
[12] Yakar S, Liu JL, Stannard B, et al. Normal growth and development in the absence of hepatic insulin-like growth factor I. Proc Natl Acad Sci U S A., 1999, 96: 7324-7329.
[13] Fujii H, Kawada N. Inflammation and fibrogenesis in steatohepatitis.. J Gastroenterol, 2012, 47: 215-225.
[14] Sanz S, Pucilowska JB, Liu S, et al. Expression of insulin-like growth factor I by activated hepatic stellate cells reduces fibrogenesis and enhances regeneration after liver injury. Gut, 2005, 54: 134-141.
[15] Skrtic S, Wallenius V, Ekberg S, et al. Insulin-like growth factors stimulate expression of hepatocyte growth factor but not transforming growth factor beta1 in cultured hepatic stellate cells. Endocrinology, 1997, 138: 4683-4689.
[16] Nishizawa H, Iguchi G, Fukuoka H, et al. IGF-I induces senescence of hepatic stellate cells and limits fibrosis in a p53-dependent manner. Sci Rep, 2016, 6:34605.
[17] Krizhanovsky V, Yon M, Dickins RA, et al. Senescence of activated stellate cells limits liver fibrosis. Cell, 2008, 134: 657-667.
[18] Handayaningsih AE, Takahashi M, Fukuoka H, et al. IGF-I enhances cellular senescence via the reactive oxygen species-p53 pathway. Biochem Biophys Res Commun,2012, 425: 478-484.
[19] Matsumoto R, Fukuoka H, Iguchi G, et al. Accelerated telomere shortening in acromegaly; IGF-I induces telomere shortening and cellular senescence. PLoS One,2015, 10: e0140189.
[20] Conchillo M, de Knegt RJ, Payeras M, et al. Insulin-like growth factor I (IGF-I) replacement therapy increases albumin concentration in liver cirrhosis: results of a pilot randomized controlled clinical trial. J Hepatol, 2006, 43: 630-636.
[21] Picardi A, de Oliveira AC, Muguerza B, et al. Low doses of insulin-like growth factor-I improve nitrogen retention and food efficiency in rats with early cirrhosis. J Hepatol,1997, 26: 191-202.
[22] Castilla-Cortázar, Pascual M, Urdaneta E, et al. Jejunal microvilli atrophy and reduced sugar transport in rats with advanced liver cirrhosis: improvement by insulin-like growth factor (IGF-I). J Hepatol, 2004, 28: 1-9.
[23] Garcia-Fernandez M, Delgado G, Puche JE, et al. Low doses of insulin-like growth factor I improve insulin resistance, lipid metabo-lism, and oxidative damage in aging rats. Endocrinology,2008;149: 2433-2442.
[24] Pascual M, Castilla-Cortazar I, Urdaneta E, et al. Altered intestinal transport of amino acids in cirrhotic rats: the effect of insulin-like growth factor-I. Am J Physiol Gastrointest Liver Physiol, 2000, 279: G319-324.
[25] Pérez R, Castilla-Cortázar I, Núez M, et al. IGF-I does not improve fat malabsorption in cirrhotic rats. J Physiol, 2001, 57: 59-60.
[26] Cemborain A, Castilla-Cortázar I, García M, et al. Osteopenia in rats with liver cirrhosis: beneficial effects of IGF-I treatment. J Hepatol, 1998, 28: 122-131.
[27] Lorenzo-zúñiga V, Rodríguez-ortigosa CM, Bartolí R, et al. Insulin-like growth factor I improves intestinal barrier function in cirrhotic rats. Gut, 2006, 55: 1306-1312..
[28] Castilla-Cortazar I, Garcia M, Muguerza B, et al. Hepatoprotective effects of insulin-like growth factor I in rats with carbon tetrachloride-induced cirrhosis. Hepatology,1997, 113: 1682-1691.
[29] Garciafernandez M, Sierra I, Puche JE, et al. Liver mitochondrial dysfunction is reverted by insulin-like growth factor II (IGF-II) in aging rats. J Transl Med, 2011, 9: 1-9.
[30] Conchillo M, de Knegt RJ, Payeras M, et al. Insulin-like growth factor I (IGF-I) replacement therapy increases albumin concentration in liver cirrhosis: results of a pilot randomized controlled clinical trial. J Hepatol, 2006, 43: 630-636. |
