Decreased mortality associated with statin treatment in patients with acute myocardial infarction and lymphotoxin-alpha C804A polymorphism.

[1]  P. Libby.  Inflammation in Atherosclerosis , 2012, Arteriosclerosis, thrombosis, and vascular biology.

[2]  I. Komuro,et al.  Endoplasmic reticulum stress as a therapeutic target in cardiovascular disease. , 2010, Circulation research.

[3]  Paul T. Williams,et al.  Genome-Wide Association of Lipid-Lowering Response to Statins in Combined Study Populations , 2010, PloS one.

[4]  Yusuke Nakamura,et al.  SNPs in BRAP associated with risk of myocardial infarction in Asian populations , 2009, Nature Genetics.

[5]  Toshihiro Tanaka,et al.  Lymphotoxin-alpha3 mediates monocyte-endothelial interaction by TNFR I/NF-kappaB signaling. , 2009, Biochemical and biophysical research communications.

[6]  M. Hori,et al.  Inhibition of Cardiac Remodeling by Pravastatin Is Associated with Amelioration of Endoplasmic Reticulum Stress , 2008, Hypertension Research.

[7]  M. Hori,et al.  Up-regulation of cell adhesion molecule genes in human endothelial cells stimulated by lymphotoxin alpha: DNA microarray analysis. , 2008, Journal of atherosclerosis and thrombosis.

[8]  Elena Galkina,et al.  Vascular adhesion molecules in atherosclerosis. , 2007, Arteriosclerosis, thrombosis, and vascular biology.

[9]  K. Eagle,et al.  Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. , 2007, JAMA.

[10]  Yusuke Nakamura,et al.  A functional SNP in PSMA6 confers risk of myocardial infarction in the Japanese population , 2006, Nature Genetics.

[11]  水野 裕八.  Impact of atherosclerosis-related gene polymorphisms on mortality and recurrent events after myocardial infarction , 2006 .

[12]  Hong Jiang,et al.  Fluvastatin inhibits the expression of tumor necrosis factor-alpha and activation of nuclear factor-kappaB in human endothelial cells stimulated by C-reactive protein. , 2005, Clinica chimica acta; international journal of clinical chemistry.

[13]  M. Vázquez-Carrera,et al.  Atorvastatin improves peroxisome proliferator-activated receptor signaling in cardiac hypertrophy by preventing nuclear factor-kappa B activation. , 2005, Biochimica et biophysica acta.

[14]  M. Pfeffer,et al.  C-reactive protein levels and outcomes after statin therapy. , 2005, The New England journal of medicine.

[15]  M. Hori,et al.  Prolonged Endoplasmic Reticulum Stress in Hypertrophic and Failing Heart After Aortic Constriction: Possible Contribution of Endoplasmic Reticulum Stress to Cardiac Myocyte Apoptosis , 2004, Circulation.

[16]  T. Wilt,et al.  Effectiveness of statin therapy in adults with coronary heart disease. , 2004, Archives of internal medicine.

[17]  M. Hori,et al.  Reduced collateral circulation to the infarct-related artery in elderly patients with acute myocardial infarction. , 2004, Journal of the American College of Cardiology.

[18]  Yusuke Nakamura,et al.  Functional variation in LGALS2 confers risk of myocardial infarction and regulates lymphotoxin-α secretion in vitro , 2004, Nature.

[19]  C. Napoli,et al.  Statin effects beyond lipid lowering--are they clinically relevant? , 2003, European heart journal.

[20]  R. Leboeuf,et al.  Loss of Lymphotoxin-α but Not Tumor Necrosis Factor-α Reduces Atherosclerosis in Mice* , 2002, The Journal of Biological Chemistry.

[21]  T. Awata,et al.  Fibrate and Statin Synergistically Increase the Transcriptional Activities of PPARα/RXRα and Decrease the Transactivation of NFκB , 2002 .

[22]  P. Hansen,et al.  Diverse effects of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase on the expression of VCAM-1 and E-selectin in endothelial cells. , 2001, The Biochemical journal.

[23]  Yoshiji Yamada,et al.  Association of the C–509→T polymorphism, alone or in combination with the T869→C polymorphism, of the transforming growth factor-β1 gene with bone mineral density and genetic susceptibility to osteoporosis in Japanese women , 2001, Journal of Molecular Medicine.

[24]  B. Aggarwal,et al.  Cloning and expression of cDNA for human lymphotoxin, a lymphokine with tumour necrosis activity , 1984, Nature.

[25]  G. Granger,et al.  Lymphocyte Cytotoxicity in vitro: Activation and Release of a Cytotoxic Factor , 1968, Nature.

[26]  B. Waksman,et al.  Cytotoxic Effect of Lymphocyte-Antigen Interaction in Delayed Hypersensitivity , 1967, Science.

[27]  B. Gersh.  Association Between Adoption of Evidence-Based Treatment and Survival for Patients With ST-Elevation Myocardial Infarction , 2012 .

[28]  The Procardis Consortium.  A trio family study showing association of the lymphotoxin-α N26 (804A) allele with coronary artery disease , 2004, European Journal of Human Genetics.

[29]  H. Nonogi,et al.  Association analysis between polymorphisms of the lymphotoxin-alpha gene and myocardial infarction in a Japanese population. , 2004, Atherosclerosis.

[30]  L. Lerman,et al.  Statin effects beyond lipid lowering--are they clinically relevant? , 2003, European heart journal.

[31]  Y. Ohnishi,et al.  Functional SNPs in the lymphotoxin-α gene that are associated with susceptibility to myocardial infarction , 2003, Nature Genetics.

[32]  T. Awata,et al.  Fibrate and statin synergistically increase the transcriptional activities of PPARalpha/RXRalpha and decrease the transactivation of NFkappaB. , 2002, Biochemical and biophysical research communications.

[33]  R. Leboeuf,et al.  Loss of lymphotoxin-alpha but not tumor necrosis factor-alpha reduces atherosclerosis in mice. , 2002, The Journal of biological chemistry.