References
Amano, M., Fukata, Y., and Kaibuchi, K. (2000). Regulation and functions of Rho-associated kinase. Exp. Cell. Res. 261(1):44–51.
Crisby, M., Nordin-Fredriksson, G., Shah, P. K., Yano, J., Zhu, J., and Nilsson, J. (2001). Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: Implications for plaque stabilization. Circulation 103:926–933.
Dangas, G., Smith, D. A., Unger, A. H., Shao, J. H., Meraj, P., Fier, C., Cohen, A. M., Fallon, J. T., Badimon, J. J., and Ambrose, J. A. (2000). Pravastatin: An antithrombotic effect independent of the cholesterol-lowering effect. Thromb Haemost. 83:688–692.
Essig, M., Nguyen, G., Prie, D., Escoubet, B., Sraer, J. D., and Friedlander, G. 1998. 3-Hydroxy-3-methylglutaryl coenzyme Areductase inhibitors increase fibrinolytic activity in rat aortic endothelial cells. Role of geranylgeranylation and Rho proteins. Circ. Res. 83:683-690.
Goldstein, J. L., and Brown, M. S. (1990). Regulation of the mevalonate pathway. Nature 343(6257):425–430.
Kalinowski, L., Dobrucki, L. W., Brovkovych, V., and Malinski, T. (2002). Increased nitric oxide bioavailability in endothelial cells contributes to the pleiotropic effect of cerivastatin. Circulation 105:933–938.
Kowluru, A., Li, G., Rabaglia, M. E., Segu, V. B., Hofmann, F., Aktories, K., and Metz, S. A. (1997). Evidence for differential roles of the Rho subfamily of GTP-binding proteins in glucose- and calcium-induced insulin secretion from pancreatic beta cells. Biochem. Pharmacol. 54(10):1097–1108.
Laufs, U., and Liao, J. K. (1998). Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. J. Biol. Chem. 273(37):24266–24271.
LIPID (Long-Term Intervention with Pravastatin in Ischaemic Disease) Study Group (1998). Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. New Engl. J. Med. 339:1349-1357.
Maher, V. M., and Thompson, G. R. (1990). HMG CoA reductase inhibitors as lipid-lowering agents: Five years experience with lovastatin and an appraisal of simvastatin and pravastatin. Quart. J. Med. 74:165–175.
Penny, W. F., Ben-Yehuda, O., Kuroe, K., Long, J., Bond, A., Bhargava, V., Peterson, J. F., McDaniel, M., Juliano, J., Witztum, J. L., Ross, J. Jr., and Peterson, K. L. (2001). Improvement of coronary artery endothelial dysfunction with lipid-lowering therapy: Heterogeneity of segmental response and correlation with plasma-oxidized low density lipoprotein. J. Am. Coll. Cardiol. 37:766-774.
Sacks, F. M., Pfeffer, M. A., Moye, L. A., Rouleau, J. L., Rutherford, J. D., Cole, T. G., Brown, L., Warnica, J. W., Arnold, J. M., Wun, C. C., Davis, B. R., and Braunwald, E. (1996). The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and recurrent events trial investigators. New Engl. J. Med. 335:1001–1009.
Scandinavian Simvastatin Survival Study Group (1994). Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). Lancet 344:1383–1389.
Shepherd, J., Cobbe, S. M., Ford, I., Isles, C. G., Lorimer, A. R., MacFarlane, P. W., McKillop, J. H., and Packard, C. J. (1995). Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. New Engl. J. Med. 333:1301–1307.
Van Aelst, L., and D’Souza-Schorey, C. (1997). Rho GTPases and signaling networks. Genes Dev. 11(18):2295–2322.
Vincent, L., Soria, C., Mirshahi, F., Opolon, P., Mishal, Z., Vannier, J. P., Soria, J., and Hong, L. (2002). Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase, inhibits endothelial cell proliferation induced by angiogenic factors in vitro and angiogenesis in in vivo models. Arterioscl. Thromb Vasc. Biol. 22:623–629.
Wagner, A. H., Kohler, T., Ruckschloss, U., Just, I., and Hecker, M. (2000). Improvement of nitric oxide-dependent vasodilatation by HMG-CoA reductase inhibitors through attenuation of endothelial superoxide anion formation. Arterioscl. Thromb Vasc. Biol. 20(1):61–69.
West of Scotland Coronary Prevention Study (1998). Influence of pravastatin and plasma lipids on clinical events in the West of Scotland Coronary Prevention Study (WOSCOPS). Circulation 97:1440–1445.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Oliyarnyk, O., Renner, W., Paulweber, B. et al. Interindividual Differences of Response to Statin Treatment Cannot Be Explained by Variations of the Human Gene for RhoA. Biochem Genet 43, 143–148 (2005). https://doi.org/10.1007/s10528-005-1507-0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/s10528-005-1507-0