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References
Weber, K.T., Cardiac interstititum. In Heart Failure: Scientific Principles and Clinical Practice, Poole-Wilson, P.A., Colucci, W.S., Massie, B.M., Chatterjee, K., Coats, A.J.S. eds. New York NY: Churchill Livingstone, 1997: p. 13–31.
Laurent, G. J., Dynamic state of collagen: pathways of collagen degradation in vivo and their possible role in regulation of collagen mass. Am J Physiol, 1987.252: p. C1–9.
Sun, Y., et al., Fibrous tissue and angiotensin II. J Mol Cell Cardiol, 1997.29: p. 2001–12.
Border, W. A. and N. A. Noble, Transforming growth factor beta in tissue fibrosis. N Engl J Med, 1994. 331: p. 1286–92.
Greenberg, B., Treatment of heart failure: state of the art and prospectives. J Cardiovasc Pharmacol, 2001. 38Suppl 2: p. S59–63.
Zaman, M.A., S. Oparil, and D.A. Calhoun, Drugs targeting the renin-angiotensinaldosterone system. Nat Rev Drug Discov, 2002. 1: p. 621–36.
Rocha, R., et al., Aldosterone: a mediator of myocardial necrosis and renal arteriopathy. Endocrinology, 2000. 141: p. 3871–8.
Modena, M.G., et al., Aldosterone inhibition limits collagen synthesis and progressive left ventricular enlargement after anterior myocardial infarction. Am Heart J, 2001.141: p. 41–6.
Leonetti, G. and C. Cuspidi, Choosing the right ACE inhibitor. A guide to selection. Drugs, 1995. 49: p. 516–35.
Fabris, B., et al., Increased cardiac angiotensin-converting enzyme in rats with chronic heart failure. Clin Exp Pharmacol Physiol, 1990. 17: p. 309–14.
Fabris, B., et al., Characterization of cardiac angiotensin converting enzyme (ACE) and in vivo inhibition following oral quinapril to rats. Br J Pharmacol, 1990. 100: p. 651–5.
Anon., Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med, 1991.325: p. 293–302.
Anon., Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med, 1992. 327: p. 669–677.
Pfeffer, M.A., et al., Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med, 1992. 327: p. 669–77.
St John Sutton, M., et al., Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial. Circulation, 1997. 96: p. 3294–9.
Konstam, M.A., et al., Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dysfunction in patients with heart failure. SOLVD Investigators. Circulation, 1992. 86: p. 431–8.
Weber, K.T., Extracellular matrix remodeling in heart failure: a role for de novo angiotensin II generation. Circulation, 1997. 96: p. 4065–82.
Weber, K.T., et al., Angiotensin II and extracellular matrix homeostasis. Int J Biochem Cell Biol, 1999. 31: p. 395–403.
Weber, K.T., Angiotensin II and connective tissue: homeostasis and reciprocal regulation. RegulPept, 1999. 82: p. 1–17.
Brilla, C.G., L.S. Matsubara, and K.T. Weber, Anti-aldosterone treatment and the prevention of myocardial fibrosis in primary and secondary hyperaldosteronism. J Mol Cell Cardiol, 1993. 25: p. 563–75.
Pitt, B., et al., The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med, 1999. 341: p. 709–17.
Zannad, F., et al., Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Rales Investigators. Circulation, 2000. 102: p. 2700–6.
Park, J.B. and E.L. Schiffrin, Cardiac and vascular fibrosis and hypertrophy in aldosteroneinfused rats: role of endothelin-1. Am J Hypertens, 2002. 15: p. 164–9.
Ogata, T., et al., Stimulation of peroxisome-proliferator-activated receptor alpha (PPAR alpha) attenuates cardiac fibrosis and endothelin-1 production in pressure-overloaded rat hearts. Clin Sci, 2002. 103: p. 284S–288S.
Rhaleb, N.E., et al., Effect of N-acetyl-seryl-aspartyl-lysyl-proline on DNA and collagen synthesis in rat cardiac fibroblasts. Hypertension, 2001. 37: p. 827–32.
Fraccarollo, D., et al., Collagen accumulation after myocardial infarction: effects of ETA receptor blockade and implications for early remodeling. Cardiovasc Res, 2002.54: p. 559–67.
Huse, M., et al., The TGF beta receptor activation process: an inhibitor-to substratebinding switch. Mol Cell, 2001. 8: p. 671–82.
Hao, J., et al., Elevation of expression of Smads 2,3, and 4, decorin and TGF-beta in the chronic phase of myocardial infarct scar healing. J Mol Cell Cardiol, 1999. 31: p. 667–78.
Laping, N.J., et al., Inhibition of transforming growth factor (TGF)-betal-induced extracellular matrix with a novel inhibitor of the TGF-beta type I receptor kinase activity: SB-431542. Mol Pharmacol, 2002. 62: p. 58–64.
Rodriguez-Barbero, A., et al., Transforming growth factor-betal induces collagen synthesis and accumulation via p38 mitogen-activated protein kinase (MAPK) pathway in cultured L(6)E(9) myoblasts. FEBS Lett, 2002. 513: p. 282–8.
McGaha, T.L., et al., Halofuginone, an inhibitor of type-I collagen synthesis and skin sclerosis, blocks transforming-growth-factor-beta-mediated Smad3 activation in fibroblasts. J Invest Dermatol, 2002. 118: p. 461–70.
Dhalla, A.K., et al., chk-YB-1b, a Y-box binding protein activates transcription from rat alpha1 (I) procollagen gene promoter. Biochem J, 1998. 336: p. 373–9.
Norman, J.T., et al., The Y-box binding protein YB-1 suppresses collagen alpha 1(1) gene transcription via an evolutionarily conserved regulatory element in the proximal promoter. J Biol Chem, 2001. 276: p. 29880–90.
Agrawal, S., Importance of nucleotide sequence and chemical modifications of antisense oligonucleotides. Biochim Biophys Acta, 1999. 1489: p. 53–68.
Opalinska, J.B. and A.M. Gewirtz, Nucleic-acid therapeutics: basic principles and recent applications. Nat Rev Drug Discov, 2002. 1: p. 503–14.
Giovannangeli, C. and C. Helene, Triplex-forming molecules for modulation of DNA information processing. Curr Opin Mol Ther, 2000. 2: p. 288–96.
Knauert, M.P. and P.M. Glazer, Triplex forming oligonucleotides: sequence-specific tools for gene targeting. Hum Mol Genet, 2001. 10: p. 2243–51.
Guntaka, R.V., B.R. Varma, and K.T. Weber, Triplex-forming oligonucleotides as modulators of gene expression. Int J Biochem Cell Biol, 2003. 35: p. 22–31.
Roque, F., et al,, Safety of intracoronary administration of c-myc antisense oligomers after percutaneous transluminal coronary angioplasty (PTCA). Antisense Nucleic Acid Drug Dev, 2001. 11: p. 99–106.
Kutryk, M.J., et al., Local intracoronary administration of antisense oligonucleotide against c-myc for the prevention of in-stent restenosis: results of the randomized investigation by the Thoraxcenter of antisense DNA using local delivery and IVUS after coronary stenting trial. J Am Coll Cardiol, 2002. 39: p. 281–7.
Swamynathan, S.K., et al., Targeted disruption of one allele of the Y-box protein gene, Chk-YB-1b, in DT40 cells results in major defects in cell cycle. Biochem Biophys Res Commun, 2002. 296: p. 451–7.
Weiss, R.H. and C.J. Randour, Attenuation of matrix protein secretion by antisense oligodeoxynucleotides to the cyclin kinase inhibitor p21(Waf1/Cip1). Atherosclerosis, 2002. 161: p. 105–12.
Kovacs, A., et al., Triple helix-forming oligonucleotide corresponding to the polypyrimidine sequence in the rat alpha 1 (I) collagen promoter specifically inhibits factor binding and transcription. J Biol Chem, 1996. 271: p. 1805–12.
Joseph, J., et al., Antiparallel polypurine phosphorothioate oligonucleotides form stable triplexes with the rat alpha1(I) collagen gene promoter and inhibit transcription in cultured rat fibroblasts. Nucleic Acids Res, 1997. 25: p. 2182–8.
Nakanishi, M., K.T. Weber, and R. V. Guntaka, Triple helix formation with the promoter of human alpha1(I) procollagen gene by an antiparallel triplex-forming oligodeoxyribonucleotide. Nucleic Acids Res, 1998. 26: p. 5218–22.
Franklin, T.J., et al., Inhibition of prolyl 4-hydroxylase in vitro and in vivo by members of a novel series of phenanthrolinones. Biochem J, 2001. 353: p. 333–8.
Nwogu, J.I., et al., Inhibition of collagen synthesis with prolyl 4-hydroxylase inhibitor improves left ventricular function and alters the pattern of left ventricular dilatation after myocardial infarction. Circulation, 2001. 104: p. 2216–21.
Siddiqui-Jain, A., et al., Direct evidence for a G-quadruplex in a promoter region and its targeting with a small molecule to repress c-MYC transcription. Proc Natl Acad Sci U S A, 2002. 99: p.11593–8.
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Guntaka, R.V., Weber, K.T. (2005). Molecular Strategies for the Prevention of Cardiac Fibrosis. In: Villarreal, F.J. (eds) Interstitial Fibrosis in Heart Failure. Developments in Cardiovascular Medicine, vol 253. Springer, New York, NY. https://doi.org/10.1007/0-387-22825-X_16
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