ライフサイエンスコーパス: HMG-CoA reductase inhibitor

1 ne monooxygenase inhibitor), or pravastatin (HMG-CoA reductase inhibitor).

2 ere treated with and without simvastatin, an HMG-CoA reductase inhibitor.

3 idemia in mild to moderate CKD patients with HMG-CoA reductase inhibitors.

4 ing pathway constitutes a novel function for HMG-CoA reductase inhibitors.

5 Collectively, these findings indicate that HMG-CoA reductase inhibitors act through a Ras farnesyla

6 A recent study suggests that pravastatin, an HMG-CoA reductase inhibitor, also decreases the incidenc

7 ese results suggest that lipid lowering with HMG-CoA reductase inhibitors alters plaque biology by re

8 These data indicate that HMG-CoA reductase inhibitors ameliorate atherosclerosis

9 Vitamin E, HMG-CoA reductase inhibitors and Ca2+ blockers each inhi

10 eased was directly related to treatment with HMG-CoA reductase inhibitors and the resulting serum LDL

11 All study subjects also received an HMG-CoA reductase inhibitor, and prophylaxis for cytomeg

12 atients (70 percent) received treatment with HMG-CoA reductase inhibitors, and 44 patients (30 percen

13 stent with known immunomodulatory actions of HMG-CoA reductase inhibitors, and the effects of calcium

14 of antiviral and proviral agents, including HMG-CoA reductase inhibitors (antiviral) and corticoster

15 he blood flow and neuroprotective effects of HMG-CoA reductase inhibitors are completely absent in eN

16 These results provide evidence that HMG-CoA reductase inhibitors are potent and effective ca

17 HMG-CoA reductase inhibitors are reported to provide saf

18 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors are powerful cholesterol-l

19 The 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are widely prescribed for

20 Statins (HMG-CoA reductase inhibitors) are the most prescribed cl

21 Statins (HMG-CoA reductase inhibitors) are used widely for the tr

22 ents, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are shown to interfere wi

23 dy of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors as potential therapy for p

24 the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors atorvastatin and simvastat

25 Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine hear

26 Prophylactic treatment with HMG-CoA reductase inhibitors augments cerebral blood flo

27 he design and synthesis of a novel series of HMG-CoA reductase inhibitors based upon a substituted py

28 To determine whether HMG CoA reductase inhibitors can prevent hypoxia-mediate

29 These data suggest that HMG-CoA reductase inhibitors can both inhibit cell proli

30 ion, it has been shown in vitro that several HMG-CoA reductase inhibitors can decrease HCV RNA replic

31 and O2- in endothelium after exposure to the HMG-CoA reductase inhibitor cerivastatin were undertaken

32 tDNA transcription; second, that a subset of HMG-CoA reductase inhibitors, combined with propranolol,

33 HMG-coA reductase inhibitors, commonly known as statins,

34 synthesis of the delta-lactone moiety of the HMG-CoA reductase inhibitors compactin and mevinolin.

35 We hypothesized that HMG-CoA reductase inhibitors decrease exocytosis of Weib

36 ether 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, described as inhibitors o

37 l components of red mold fermented products, HMG-CoA reductase inhibitors, did not exacerbate pre-exi

38 Statins, a class of HMG-CoA reductase inhibitors, display pleiotropic immuno

39 In conclusion, atorvastatin, and likely all HMG-CoA reductase inhibitors, does not inhibit HCV RNA r

40 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, e.g., simvastatin, have b

41 ographic progression and the benefits of the HMG-CoA reductase inhibitor fluvastatin in patients with

42 patients were medicated with aspirin and an HMG-CoA reductase inhibitor for >/=6 weeks before enteri

43 study of fluvastatin, pravastatin, and other HMG-CoA reductase inhibitors for the prevention of GVD i

44 using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors for patients after MI; usi

45 demonstrated the potential of lovastatin, a HMG-CoA reductase inhibitor, for the restoration of impa

46 hen administered at a high dosage (including HMG-CoA reductase inhibitors >75 mg/day/adult).

47 t clinically relevant doses, simvastatin, an HMG-CoA reductase inhibitor, has been shown to lower ser

48 HMG-CoA reductase inhibitors have been shown to upregula

49 s, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have anti-inflammatory ef

50 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (HRIs) were found incident

51 Interactions between UCN-01 and HMG-CoA reductase inhibitors (ie, statins) have been exa

52 ng of antiviral activity associated with the HMG-CoA reductase inhibitors implies an important role f

53 that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase inhibitors improve endothelium-depend

54 ts explain some of the beneficial effects of HMG-CoA reductase inhibitors in cardiac transplantation.

55 ials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, in the form of statins, h

56 chanism by which 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors increase endothelial nitri

57 in, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor, induced apoptosis in human

58 Finally, HMG-CoA reductase inhibitors inhibited signaling by vasc

59 HMG-CoA reductase inhibitors interfered with angiogenesi

60 The up-regulation of eNOS by HMG-CoA reductase inhibitors is not associated with chan

61 e, indicating that enhanced eNOS activity by HMG-CoA reductase inhibitors is the predominant if not t

62 Simvastatin, an HMG-coA reductase inhibitor, is known to attenuate infla

63 the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors known as statins have anti

64 Orally administered cholesterol-lowering HMG-CoA reductase inhibitors (known as statins), which e

65 mouse model of NF1 has been treated with the HMG-CoA reductase inhibitor lavastatin, which improves t

66 Depleting endogenous cholesterol with the HMG CoA reductase inhibitor lovastatin leads to a 2-fold

67 dominant-negative AKT, or treatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT ph

68 The hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor lovastatin depletes cellula

69 et al., in this issue, demonstrates that the HMG-CoA reductase inhibitor lovastatin can normalize pro

70 dermal tumors we evaluated the effect of the HMG-CoA reductase inhibitor lovastatin on the Ewing's sa

71 Treatment of pregnant mice with the HMG-CoA reductase inhibitor lovastatin reduced sterol sy

72 Three negative growth regulators, the HMG-CoA reductase inhibitor lovastatin, the antimetaboli

73 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin induces growth a

74 -lowering hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin, the dihydropyri

75 LDLR SRE was observed in the presence of the HMG-CoA reductase inhibitor, lovastatin, when PP2A activ

76 prostate (TRAMP cells) were treated with the HMG-CoA reductase inhibitor, lovastatin.

77 NA stability and suggest that treatment with HMG CoA reductase inhibitors may have beneficial effects

78 These findings suggest that HMG CoA reductase inhibitors may have beneficial effects

79 ial exocytosis is a novel mechanism by which HMG-CoA reductase inhibitors may reduce vascular inflamm

80 ch as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, may prevent the developme

81 uman endothelial cells were treated with the HMG-CoA reductase inhibitor, mevastatin (1-10 microM), i

82 ive study designed to evaluate the effect of HMG-CoA reductase inhibitors on atherosclerosis.

83 HMG-CoA reductase inhibitors or statins are associated w

84 ls of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy have dem

85 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

86 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolera

87 ugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins, are used in th

88 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

89 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, target liver

90 Fluvastatin, the first entirely synthetic HMG-CoA reductase inhibitor, possesses a distinct pharma

91 m the 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor pravastatin.

92 Recent studies suggest that HMG-CoA reductase inhibitors promote vascular endothelia

93 ay represent an important mechanism by which HMG-CoA reductase inhibitors protect against the develop

94 Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors protect the vasculature fr

95 lowering agents, 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, protect against cerebral

96 Our results suggest that HMG-CoA reductase inhibitors provide a prophylactic trea

97 Lipid lowering with HMG-CoA reductase inhibitors reduces acute coronary even

98 These results indicate that HMG CoA reductase inhibitors regulate ecNOS function and

99 Although HMG CoA reductase inhibitors restore endothelial functio

100 The HMG-CoA reductase inhibitors result in substantial reduc

101 To test whether lipid lowering with an HMG-CoA reductase inhibitor retards macrophage accumulat

102 e effects of diabetes and treatment with the HMG-CoA reductase inhibitor rosuvastatin (RSV) were exam

103 These data indicate that the HMG-CoA reductase inhibitor rosuvastatin has a favorable

104 novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, rosuvastatin, on endotheli

105 Furthermore, HMG-CoA reductase inhibitors significantly decreased all

106 f cholesterol biosynthesis using statins (an HMG-CoA reductase inhibitor) significantly increased the

107 xposed to hypoxia (3% O2) in the presence of HMG CoA reductase inhibitors simvastatin and lovastatin

108 stances 12 to 16 nmol/mg) in the presence of HMG CoA reductase inhibitors simvastatin and lovastatin.

109 receive either vehicle or treatment with the HMG-CoA reductase inhibitor simvastatin (2 mg/kg per day

110 iposomes ([S]-LIP), that are loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evalua

111 In vivo, the HMG-CoA reductase inhibitor simvastatin dose-dependently

112 In this study, we analyzed the effect of the HMG-CoA reductase inhibitor simvastatin on disease manif

113 hyl-beta-cyclodextrin, 2) treatment with the HMG-CoA reductase inhibitor simvastatin, and 3) shRNA-me

114 were partially rescued by treatment with the HMG-CoA reductase inhibitor simvastatin.

115 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor simvastatin to healthy subj

116 imvastatin-treated animals in vivo, that the HMG-CoA reductase inhibitor, simvastatin, augments the c

117 transplant recipients should be treated with HMG-CoA reductase inhibitors starting early posttranspla

118 Lovastatin, an HMG-CoA reductase inhibitor (statin), was immunomodulato

119 ssive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy on surroga

120 ensin-converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors (statins) have more than do

121 that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductase inhibitors (statins) might slow aorti

122 beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) within 60 days a

123 Hydroxymethylglutaryl (HMG) CoA reductase inhibitors (statins) may favorably af

124 This study tested whether HMG-CoA reductase inhibitors (statins) alter interstitia

125 se cholesterol is a product of this pathway, HMG-CoA reductase inhibitors (statins) are used to treat

126 The HMG-CoA reductase inhibitors (statins) are widely prescr

127 plementary activity between these agents and HMG-CoA reductase inhibitors (statins) based on their ab

128 Recent evidence suggests that HMG-CoA reductase inhibitors (statins) can prevent the p

129 HMG-CoA reductase inhibitors (statins) have been shown t

130 Recent evidence suggests that HMG-CoA reductase inhibitors (statins) have beneficial e

131 There is experimental evidence to show that HMG-CoA reductase inhibitors (statins) may inhibit proli

132 HMG-CoA reductase inhibitors (statins) reduce GAD in hum

133 The ability of cholesterol lowering HMG-CoA reductase inhibitors (statins) to improve outcom

134 of low-density lipoprotein cholesterol with HMG-CoA reductase inhibitors (statins).

135 th 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) inhibitors (statins).

136 d for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are related to r

137 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

138 hough 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) can restore endo

139 ntly, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the ma

140 rative effects of hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins) on oxidative str

141 etimibe) and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins) provides a power

142 Three-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) reduce coronary

143 RBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), and selective s

144 esults of eight recently published trials of Hmg CoA reductase inhibitors ("statins") on the conclusi

145 nt of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors--"statins." Initial studie

146 HMG-CoA reductase inhibitors such as statins are cholest

147 It is unclear whether the addition of an HMG-CoA reductase inhibitor to interferon or a more pote

148 egatively regulates eNOS expression and that HMG-CoA reductase inhibitors up-regulate eNOS expression

149 with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors was begun at the discretio

150 ockers and hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors were shown to decrease cor

151 tins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, which are approved for ch

152 angiogenesis and an antiangiogenic effect of HMG-CoA reductase inhibitors with possible important the