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

4 idemia in mild to moderate CKD patients with 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 eptor (IGF1R) inhibitor, and fluvastatin, an HMG-CoA reductase inhibitor, as potential chemopreventiv

25 ed with the PKG activator sildenafil and the HMG CoA reductase inhibitor atorvastatin to further redu

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

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

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

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

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

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

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

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

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

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

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

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

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

39 Trials involving vitamin D therapy and HMG-CoA reductase inhibitors did not demonstrate attenua

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

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

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

43 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, e.g., simvastatin, have b

44 y, regulating cholesterol metabolism with an HMG-CoA reductase inhibitor, FDA-approved atorvastatin,

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

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

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

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

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

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

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

52 HMG-CoA reductase inhibitors have been shown to upregula

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

54 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (HRIs) were found incident

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

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

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

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

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

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

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

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

63 HMG-CoA reductase inhibitors interfered with angiogenesi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 HMG-CoA reductase inhibitors or statins are associated w

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

89 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

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

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

92 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

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

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

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

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

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

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

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

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

101 PKG phosphorylates K-RAS and HMG CoA reductase inhibitors reduce K-RAS farnesylation

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

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

104 Although HMG CoA reductase inhibitors restore endothelial functio

105 The HMG-CoA reductase inhibitors result in substantial reduc

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

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

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

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

110 Furthermore, HMG-CoA reductase inhibitors significantly decreased all

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ular 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment for dysl

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

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

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

129 kers, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins), oral diabetes m

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

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

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

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

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

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

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

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

138 Suppression of cholesterol levels by HMG-CoA reductase inhibitors (statins) impaired synaptic

139 HMG-CoA reductase inhibitors (statins) improve cutaneous

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

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

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

143 anticancer and radiosensitisation effects of HMG-CoA reductase inhibitors (statins).

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

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

146 nephrine reuptake inhibitors (SSRIs, SNRIs), HMG-CoA reductase-inhibitors (statins), and angiotensin-

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

148 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

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

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

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

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

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

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

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

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

157 HMG-CoA reductase inhibitors such as statins are cholest

158 Statins are HMG-CoA reductase inhibitors that are known to inhibit c

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

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

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

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

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

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