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Chemical Compound Review

Synvinolin     [(1S,3R,7R,8S,8aS)-8-[2- [(2R,4R)-4-hydroxy...

Synonyms: Rendapid, Simvacor, Simvoget, Sinvacor, Zocor, ...
 
 
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Disease relevance of Zocor

 

Psychiatry related information on Zocor

  • Simvastatin strongly reduces levels of Alzheimer's disease beta -amyloid peptides Abeta 42 and Abeta 40 in vitro and in vivo [6].
  • Over the median follow-up period of 5.4 years, one or more major coronary events (MCEs) occurred in 622 (28%) of the 2223 patients in the placebo group and 431 (19%) of the 2221 patients in the simvastatin group (34% risk reduction, P<.00001) [7].
  • RESULTS: Simvastatin treatment not only reversed learning and memory deficits in the Tg2576 mice, but also enhanced learning and memory in the nontransgenic mice [8].
  • During biweekly assessments, four subjects on simvastatin and one on placebo experienced depressive symptoms, as manifest by Center for Epidemiological Studies Depression scale scores greater than 16 (exact P=.36) [9].
  • The study found no benefit of simvastatin therapy in preventing noncardiac events (eg, dementia, osteoporotic fractures), and no negative effects, such as an increase in cancer, respiratory disease, or suicide [10].
 

High impact information on Zocor

 

Chemical compound and disease context of Zocor

 

Biological context of Zocor

  • Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats [19].
  • The role of Akt signaling in mediating effects of statin on EPCs is suggested by the observation that simvastatin rapidly activates Akt protein kinase in EPCs, enhancing proliferative and migratory activities and cell survival [20].
  • We show here, using a chemotaxis assay of bone marrow mononuclear cells in vitro and EPC culture assay of peripheral blood from simvastatin-treated animals in vivo, that the HMG-CoA reductase inhibitor, simvastatin, augments the circulating population of EPCs [20].
  • RESULTS: In protocol 1, acute simvastatin did not modify the hepatic venous pressure gradient but increased the hepatic blood flow (21% +/- 13% at 30 minutes; P = 0.01) and decreased hepatic sinusoidal resistance by 14% +/- 11% (P = 0.04) [5].
  • Here we show that simvastatin (2 microM) inhibits clump formation and induces apoptosis of EBV-transformed LCLs [21].
 

Anatomical context of Zocor

  • Similar to vascular endothelial growth factor (VEGF) treatment, both simvastatin administration and enhanced Akt signaling in the endothelium promoted angiogenesis in ischemic limbs of normocholesterolemic rabbits [13].
  • Direct evidence that this increased pool of circulating EPCs originates from bone marrow and may enhance neovascularization was demonstrated in simvastatin-treated mice transplanted with bone marrow from transgenic donors expressing beta-galactosidase transcriptionally regulated by the endothelial cell-specific Tie-2 promoter [20].
  • Cholesterol also potentiated Akt activation in normal prostate epithelial cells, which were resistant to the apoptotic effects of simvastatin [22].
  • We treated neonatal rat cardiac myocytes with angiotensin II (AngII) with and without simvastatin (Sim) and found that Sim decreased AngII-induced protein content, [3H] leucine uptake, and atrial natriuretic factor (ANF) promoter activity [4].
  • To confirm this advantage, patients with heterozygous familial hypercholesterolaemia and coronary artery disease were randomised to receive LDL apheresis fortnightly (with disposable dextran sulphate/cellulose columns) plus simvastatin 40 mg daily, or colestipol 20 g plus simvastatin 40 mg daily [23].
 

Associations of Zocor with other chemical compounds

 

Gene context of Zocor

 

Analytical, diagnostic and therapeutic context of Zocor

References

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  2. Cost effectiveness of simvastatin treatment to lower cholesterol levels in patients with coronary heart disease. Scandinavian Simvastatin Survival Study Group. Johannesson, M., Jönsson, B., Kjekshus, J., Olsson, A.G., Pedersen, T.R., Wedel, H. N. Engl. J. Med. (1997) [Pubmed]
  3. Myositis and rhabdomyolysis associated with concurrent use of simvastatin and nefazodone. Jacobson, R.H., Wang, P., Glueck, C.J. JAMA (1997) [Pubmed]
  4. Statins as antioxidant therapy for preventing cardiac myocyte hypertrophy. Takemoto, M., Node, K., Nakagami, H., Liao, Y., Grimm, M., Takemoto, Y., Kitakaze, M., Liao, J.K. J. Clin. Invest. (2001) [Pubmed]
  5. Simvastatin enhances hepatic nitric oxide production and decreases the hepatic vascular tone in patients with cirrhosis. Zafra, C., Abraldes, J.G., Turnes, J., Berzigotti, A., Fernández, M., Garca-Pagán, J.C., Rodés, J., Bosch, J. Gastroenterology (2004) [Pubmed]
  6. Simvastatin strongly reduces levels of Alzheimer's disease beta -amyloid peptides Abeta 42 and Abeta 40 in vitro and in vivo. Fassbender, K., Simons, M., Bergmann, C., Stroick, M., Lutjohann, D., Keller, P., Runz, H., Kuhl, S., Bertsch, T., von Bergmann, K., Hennerici, M., Beyreuther, K., Hartmann, T. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  7. Lipoprotein changes and reduction in the incidence of major coronary heart disease events in the Scandinavian Simvastatin Survival Study (4S). Pedersen, T.R., Olsson, A.G., Faergeman, O., Kjekshus, J., Wedel, H., Berg, K., Wilhelmsen, L., Haghfelt, T., Thorgeirsson, G., Pyörälä, K., Miettinen, T., Christophersen, B., Tobert, J.A., Musliner, T.A., Cook, T.J. Circulation (1998) [Pubmed]
  8. Simvastatin enhances learning and memory independent of amyloid load in mice. Li, L., Cao, D., Kim, H., Lester, R., Fukuchi, K. Ann. Neurol. (2006) [Pubmed]
  9. Simvastatin causes changes in affective processes in elderly volunteers. Morales, K., Wittink, M., Datto, C., DiFilippo, S., Cary, M., TenHave, T., Katz, I.R. Journal of the American Geriatrics Society. (2006) [Pubmed]
  10. The Heart Protection Study: high-risk patients benefit from statins, regardless of LDL-C level. Gurm, H.S., Hoogwerf, B. Cleveland Clinic journal of medicine. (2003) [Pubmed]
  11. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. Brown, B.G., Zhao, X.Q., Chait, A., Fisher, L.D., Cheung, M.C., Morse, J.S., Dowdy, A.A., Marino, E.K., Bolson, E.L., Alaupovic, P., Frohlich, J., Albers, J.J. N. Engl. J. Med. (2001) [Pubmed]
  12. Estrogen and progestin compared with simvastatin for hypercholesterolemia in postmenopausal women. Darling, G.M., Johns, J.A., McCloud, P.I., Davis, S.R. N. Engl. J. Med. (1997) [Pubmed]
  13. The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals. Kureishi, Y., Luo, Z., Shiojima, I., Bialik, A., Fulton, D., Lefer, D.J., Sessa, W.C., Walsh, K. Nat. Med. (2000) [Pubmed]
  14. Rhabdomyolysis due to interaction of simvastatin with mibefradil. Schmassmann-Suhijar, D., Bullingham, R., Gasser, R., Schmutz, J., Haefeli, W.E. Lancet (1998) [Pubmed]
  15. "The lower the better" in hypercholesterolemia therapy: a reliable clinical guideline?. Jacobson, T.A. Ann. Intern. Med. (2000) [Pubmed]
  16. RhoA GTPase inactivation by statins induces osteosarcoma cell apoptosis by inhibiting p42/p44-MAPKs-Bcl-2 signaling independently of BMP-2 and cell differentiation. Fromigu??, O., Ha??, E., Modrowski, D., Bouvet, S., Jacquel, A., Auberger, P., Marie, P.J. Cell Death Differ. (2006) [Pubmed]
  17. In vivo enhanced antitumor activity of carmustine [N,N'-bis(2-chloroethyl)-N-nitrosourea] by simvastatin. Soma, M.R., Baetta, R., De Renzis, M.R., Mazzini, G., Davegna, C., Magrassi, L., Butti, G., Pezzotta, S., Paoletti, R., Fumagalli, R. Cancer Res. (1995) [Pubmed]
  18. 3-Hydroxy-3-methylglutaryl-CoA reductase inhibitors attenuate vascular smooth muscle proliferation by preventing rho GTPase-induced down-regulation of p27(Kip1). Laufs, U., Marra, D., Node, K., Liao, J.K. J. Biol. Chem. (1999) [Pubmed]
  19. Stimulation of bone formation in vitro and in rodents by statins. Mundy, G., Garrett, R., Harris, S., Chan, J., Chen, D., Rossini, G., Boyce, B., Zhao, M., Gutierrez, G. Science (1999) [Pubmed]
  20. HMG-CoA reductase inhibitor mobilizes bone marrow--derived endothelial progenitor cells. Llevadot, J., Murasawa, S., Kureishi, Y., Uchida, S., Masuda, H., Kawamoto, A., Walsh, K., Isner, J.M., Asahara, T. J. Clin. Invest. (2001) [Pubmed]
  21. Simvastatin induces apoptosis of Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and delays development of EBV lymphomas. Katano, H., Pesnicak, L., Cohen, J.I. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  22. Cholesterol targeting alters lipid raft composition and cell survival in prostate cancer cells and xenografts. Zhuang, L., Kim, J., Adam, R.M., Solomon, K.R., Freeman, M.R. J. Clin. Invest. (2005) [Pubmed]
  23. Familial Hypercholesterolaemia Regression Study: a randomised trial of low-density-lipoprotein apheresis. Thompson, G.R., Maher, V.M., Matthews, S., Kitano, Y., Neuwirth, C., Shortt, M.B., Davies, G., Rees, A., Mir, A., Prescott, R.J. Lancet (1995) [Pubmed]
  24. Comparison between simvastatin and bezafibrate in effect on plasma lipoproteins and apolipoproteins in primary hypercholesterolaemia. Schulzeck, P., Bojanovski, M., Jochim, A., Canzler, H., Bojanovski, D. Lancet (1988) [Pubmed]
  25. 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors up-regulate transforming growth factor-beta signaling in cultured heart cells via inhibition of geranylgeranylation of RhoA GTPase. Park, H.J., Galper, J.B. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  26. Circulating transcriptome reveals markers of atherosclerosis. Patino, W.D., Mian, O.Y., Kang, J.G., Matoba, S., Bartlett, L.D., Holbrook, B., Trout, H.H., Kozloff, L., Hwang, P.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
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  28. Simvastatin does not exhibit therapeutic anti-inflammatory effects in asthma. Menzies, D., Nair, A., Meldrum, K.T., Fleming, D., Barnes, M., Lipworth, B.J. J. Allergy Clin. Immunol. (2007) [Pubmed]
  29. Simvastatin suppresses self-renewal of mouse embryonic stem cells by inhibiting RhoA geranylgeranylation. Lee, M.H., Cho, Y.S., Han, Y.M. Stem. Cells (2007) [Pubmed]
  30. Simvastatin inhibits IL-17 secretion by targeting multiple IL-17-regulatory cytokines and by inhibiting the expression of IL-17 transcription factor RORC in CD4+ lymphocytes. Zhang, X., Jin, J., Peng, X., Ramgolam, V.S., Markovic-Plese, S. J. Immunol. (2008) [Pubmed]
  31. Combining simvastatin with the farnesyltransferase inhibitor tipifarnib results in an enhanced cytotoxic effect in a subset of primary CD34+ acute myeloid leukemia samples. van der Weide, K., de Jonge-Peeters, S.D., Kuipers, F., de Vries, E.G., Vellenga, E. Clin. Cancer Res. (2009) [Pubmed]
  32. Simvastatin promotes Th2-type responses through the induction of the chitinase family member Ym1 in dendritic cells. Arora, M., Chen, L., Paglia, M., Gallagher, I., Allen, J.E., Vyas, Y.M., Ray, A., Ray, P. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  33. Development and characterization of a hypomorphic Smith-Lemli-Opitz syndrome mouse model and efficacy of simvastatin therapy. Correa-Cerro, L.S., Wassif, C.A., Kratz, L., Miller, G.F., Munasinghe, J.P., Grinberg, A., Fliesler, S.J., Porter, F.D. Hum. Mol. Genet. (2006) [Pubmed]
  34. Simvastatin Potentiates TNF-{alpha}-Induced Apoptosis through the Down-Regulation of NF-{kappa}B-Dependent Antiapoptotic Gene Products: Role of I{kappa}B{alpha} Kinase and TGF-beta-Activated Kinase-1. Ahn, K.S., Sethi, G., Aggarwal, B.B. J. Immunol. (2007) [Pubmed]
  35. Modulation of the expression of connective tissue growth factor by alterations of the cytoskeleton. Ott, C., Iwanciw, D., Graness, A., Giehl, K., Goppelt-Struebe, M. J. Biol. Chem. (2003) [Pubmed]
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