ライフサイエンスコーパス: statin

1 level of impairment of islet function by the statin.

2 bjective than objective AEs are reported for statins.

3 r benefit from addition of this treatment to statins.

4 igher risk who derive increased benefit from statins.

5 ogic inhibition of the mevalonate pathway by statins.

6 pids, as well as anticarcinogenic effects of statins.

7 4.8% for clopidogrel, and 36.2% to 77.1% for statins.

8 ion to usual background therapies, including statins.

9 ts, RRs were not statistically different for statin (0.82 [0.73-0.91]) and non-statin treatment (0.67

10 e levels of vitamin D were able to adhere to statins 1 year after vitamin D supplementation.

11 eficiaries increased, with gains of 89.7% in statins (11.0 to 20.8 million), 76% in antihypertensives

12 .4% versus 52.9%, P<0.001) or high-intensity statins (15.3% versus 19.8%, P<0.01) compared with men.

13 ad a lower prevalence of prescription of any statin (48.4% versus 52.9%, P<0.001) or high-intensity s

14 On the one hand, statins abolish the insulinotropic effects of bile acids

15 ) seem to be favorable options for improving statin adherence.

16 the cardioprotective effects of intravenous statin administration during myocardial infarction (MI)

17 luate whether the high frequency of reported statin adverse effects (AEs) may be associated with the

18 Subjective statin AEs, potentially related to the nocebo effect are

19 However, whether statins affect cardiovascular function in the fetus is c

20 spirin nonsteroidal anti-inflammatory drugs, statins, agents that target metabolic pathways, and vita

21 or rosuvastatin 20 mg), and low/medium dose statins (all other statin regimens) at the time of the p

22 ion are ambiguous, making it unclear whether statins, alone or in combination, can be used for chemot

23 are the risk for ASCVD events and the use of statins among patients with PAD versus those with corona

24 be rechallenged with the same or a different statin and be adherent 1 year after a statin-related adv

25 achieve these goals, investigators used the statin and dosage of their choice and added ezetimibe as

26 In the non-statin and statin groups, 9.5 and 3.4% of participants d

27 nges in the use of aspirin, clopidogrel, and statins and 1-year cause-specific hazard ratios for adve

28 had increases in prescription rates of both statins and antihypertensives.

29 t, 44% of nonexpander states saw declines in statins and antihypertensives.

30 Mechanistically, statins and NSDHL loss induce SREBP1 activation, which p

31 f patients who were previously intolerant to statins and who had low baseline levels of vitamin D wer

32 reatment regimens, including anticoagulants, statins, and neurohormonal inhibition, were found to fur

33 s of medications in preventive drug classes (statins, antiglaucoma drugs, and beta blockers) as an ap

34 ion rates per 1000 Medicaid beneficiaries of statins, antihypertensives, P2Y12 inhibitors, and direct

35 Statins are associated with fewer postoperative cardiova

36 Statins are being studied to prevent ASCVD in human immu

37 We show that statins are effective at reducing Abeta in human neurons

38 Statins are HMG-CoA reductase inhibitors that are known

39 Statins are widely prescribed inhibitors of the mevalona

40 nents, REPRIEVE will assess the effects of a statin as a cardiovascular disease prevention strategy i

41 acterial infectivity and suggests the use of statins as tuberculosis preventive therapy by inhibiting

42 in adipose tissue of OSA patients receiving statin, aspirin, and/or RAS inhibitors was comparable to

43 Heterogeneity in statin-associated benefit was examined by sex, age, and

44 However, few studies have directly compared statin-associated benefits and harms or examined heterog

45 ontinuation is because of the development of statin-associated muscle symptoms, but a range of other

46 nd focus on the evaluation and management of statin-associated muscle symptoms.

47 ciated benefit was examined by sex, age, and statin-associated T2D relative risk (RR) (range: 1.11-1.

48 y limitation was uncertainty in estimates of statin-associated T2D risk, highlighting areas in which

49 ions shoulder the highest relative burden of statin-associated T2D risk.

50 LHH by age and sex became more pronounced as statin-associated T2D RR increased, with a majority of s

51 number of ASCVD events prevented when higher statin-associated T2D RRs were assumed (LHH range: 0.72-

52 >=70 years of age, and participants who took statins at baseline were compared with those who did not

53 ian age 74.2 years, 56.0% women), 5,629 took statins at baseline.

54 8 and 245 participants were taking high dose statins (atorvastatin 40-80 mg or rosuvastatin 20 mg), a

55 Mevalonate pathway inhibition by statins blocked pyrimidine nucleotide biosynthesis and i

56 No consensus was reached on the use of statins, but mTOR inhibitors and somatostatin analogues

57 ents with premature MI are not identified as statin candidates before their event on the basis of the

58 -lowering MEK inhibitor, in combination with statins, caused profound tumor cell death.

59 this phenotype; treatment of zebrafish with statins, cholesterol synthesis inhibitors, decreased spr

60 esterolaemic adults currently treated with a statin compared to age-matched controls.

61 nts, 63.3% were discharged on high-intensity statin compared with 48.4% for non-FH patients (p < 0.00

62 terol scavenger (beta-methylcyclodextrin) or statin compound (simvastatin) blocked ATP and IL-33 rele

63 We further show that statins decrease flAPP interaction with BACE1 and enhanc

64 This case-control study suggests that statins decrease the risk of ECC and may improve surviva

65 Altering cholesterol metabolism using statins decreased the generation of sAPPbeta and increas

66 a = 393 +/- 96%, high: Delta = 311 +/- 120%, statin: Delta = 256 +/- 90%; P = 0.11).

67 s study was to examine the association among statins, dementia-free and disability-free survival, and

68 trated that evolocumab added to a background statin did not affect cognitive performance in a subset

69 iptions (per 1000 Medicaid beneficiaries) of statins (DID estimate [95% CI]: 22.5 [16.5-28.6], P<0.00

70 The major reason for statin discontinuation is because of the development of

71 e guideline in 7 crucial areas: targeting of statin dose (not low-density lipoprotein cholesterol goa

72 h statin treatment discontinuation, nondaily statin dosing lowered total cholesterol and LDL-C levels

73 ; 91% white), 57 178 (17.5%) newly initiated statins during the study period.

74 oach (Protein Extension Assay), to determine statin effects on over 350 plasma proteins in relevant A

75 n the basis of greater guideline-recommended statin eligibility and higher rates of statin therapy.

76 age, leading to nearly universal risk-based statin eligibility in the elderly population.

77 hyl-glutaryl-coenzyme A reductase inhibitor (statin) eligibility criteria for primary prevention to i

78 Comparing statin ever users to nonusers, patients with dCCA who us

79 Beyond lipid-lowering, statins exert cardioprotective effects.

80 he independent effects of hyperlipidemia and statin exposure on mortality, hepatic decompensation, an

81 Statin exposure was not predicted to increase PD risk, a

82 ntify genetic support for the repurposing of statins, ezetimibe, or mipomersen for AD prevention.

83 th served as the validation data set (SAILS [Statins for Acutely Injured Lungs from Sepsis]; n = 745)

84 study, we screened 8 commercially available statins for cytotoxic effect, anti-TB activity, synergy

85 diabetes (T2D) risk among populations taking statins for the primary prevention of atherosclerotic ca

86 ion about Vascepa (ie, use as an add-on to a statin) from the manufacturer, and 16% had prescribed it

87 0059), and meibum quality (P = .0002) in the statin group during follow-up visits.

88 In the non-statin and statin groups, 9.5 and 3.4% of participants developed PE

89 ers to nonusers, patients with dCCA who used statins had significantly overall better survival (hazar

90 Statins have been proven to be cytotoxic to human cholan

91 hylglutaryl coenzyme A reductase inhibitors (statins) have broad anti-inflammatory and immunomodulato

92 Multiple statins impaired insulin action at the level of Akt/prot

93 e findings provide new in vivo evidence that statins improve experimental arteriovenous fistula paten

94 hibition of intestinal hyperproliferation by statins in an Apc/KrasG12D-mutant mouse model was indepe

95 The use of statins in complicated pregnancy is being considered, as

96 indicate a potential chemopreventive role of statins in epithelial ovarian cancer risk.

97 arding the benefits and harms of prescribing statins in healthy subjects >=70 years of age.

98 Given the role of statins in the reduction of systemic and pancreatic intr

99 The potential benefits of statins in this context will require further evaluation

100 Statins, in addition to their cholesterol lowering effec

101 m between January 2010 and December 2019 for statins, including, atorvastatin, lovastatin, pravastati

102 Skeletal myopathy is a known statin-induced adverse effect associated with mitochondr

103 Additionally, statin-induced changes in APP dimerization and APP-BACE1

104 Thus, statin-induced ROS production in cancer cells can be exp

105 ciated muscle symptoms, but a range of other statin-induced side effects also exist.

106 Statins' induction of multiple anti-inflammatory and ant

107 management may include the use of diuretics, statins, infection prophylaxis and anticoagulation.

108 Statins inhibit flux through this pathway, but if and ho

109 whom 13-28 million adults were eligible for statin initiation.

110 Restriction of the study population to statin initiators with an uncensored approach resulted i

111 CVD was documented in 35.6% of patients, and statin intolerance/contraindications to statin use were

112 Continuation of statins is advised, but initiating statin therapy to tre

113 is study shows that the diabetogenic risk of statins is coupled to the activity of farnesoid X recept

114 erapeutically targeted by ROCK inhibitors or statins, is a key downstream effector of RHOA GTPases.

115 ome trials confirm that, within a few years, statins lower the relative risk of major atherosclerotic

116 rove patients' tolerance of and adherence to statins may enhance the effectiveness of dyslipidemia tr

117 Statins may help prevent cardiovascular disease (CVD) in

118 nflammation, we hypothesized that the use of statins may lower the risk of PEP.

119 , adherence to a healthy lifestyle or use of statins may offset increased inherited risk.(,)

120 senchymal transition by cholesterol-lowering statins may promote the basal type of PDAC, conferring p

121 It is concluded that statin-mediated cholesterol depletion may coordinate vas

122 Altogether, it is concluded that statin-mediated cholesterol depletion may coordinate VSM

123 Proof is provided that statin-mediated cholesterol depletion remodels total vas

124 ar smooth muscle cell biomechanics following statin-mediated cholesterol depletion.

125 l orientation was reduced (-24.5%) following statin-mediated cholesterol depletion.

126 ctin cytoskeletal orientation in response to statin-mediated cholesterol depletion.

127 Nonetheless, the effect of statin-mediated cholesterol management on cellular biome

128 ting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants.

129 ducted in participants who were not taking a statin medication at the time of ERCP, while 363 partici

130 Among patients with coronary artery disease, statin medication rates increased from 66% to 80.1%.

131 time of ERCP, while 363 participants were on statin medications at the time of ERCP; 118 and 245 part

132 Specifically, statins mitigated adhesion and spreading abnormalities w

133 A polypill comprising statins, multiple blood-pressure-lowering drugs, and asp

134 Possible rescue therapies (high-dose statins, octreotide, thalidomide, lenalidomide, and tamo

135 but no studies investigated the effect of a statin on atherogenesis affected by severe periodontitis

136 ve been reported which studied the impact of statins on (a) whether they can worsen glucose tolerance

137 but little is known regarding the effects of statins on a broad range of inflammatory and cardiovascu

138 in vivo physiologic and molecular effects of statins on fistula patency and maturation remain poorly

139 ing and plays a role for negative effects of statins on glycemic control.

140 We examined the effects of statins on hyperglycemia, glucose tolerance, fatty acid

141 We show that the effect estimates of statins on metabolites from the cross-sectional study ar

142 eneficial effect of anti-diabetic agents and statins on outcomes in heart failure patients without at

143 Nonetheless, reported effects of statins on tumor progression are ambiguous, making it un

144 trometry and isotope tracing, we showed that statins only modestly affected cancer cholesterol homeos

145 Notably, a history of statin or SSRI usage reduced the risk of EAC or HGD by 4

146 new incident CLI are less likely to receive statin or undergo revascularization at 90 days compared

147 ssion was attenuated with concomitant use of statins or corticosteroids.

148 and rechallenge with the same or a different statin (or a lower dose) seem to be favorable options fo

149 al therapies, including aspirin (p < 0.001), statin (p < 0.001), and beta-blockers (p = 0.002).

150 drug classes: HMGCR (encoding the target for statins), PCSK9 (encoding the target for PCSK9 inhibitor

151 3.7% vs. 43.7%, p = 0.99) or higher rates of statin prescriptions (25.0% vs. 23.8%, p = 0.04).

152 Statin prescriptions increased from 47.4% in 2005 to 60.

153 Lipophilic statins prevent membrane association and activity of Rab

154 Our data indicate that statins reduce Abeta production by decreasing BACE1 inte

155 Our results predict that statins reduce cancer risk but other lipid-lowering trea

156 This suggests that statins reduce cancer risk through a cholesterol indepen

157 Low-, moderate-, and high-intensity statin regimens were used by 751 subjects (1.9%), 2,655

158 mg), and low/medium dose statins (all other statin regimens) at the time of the procedure, respectiv

159 ferent statin and be adherent 1 year after a statin-related adverse event led to discontinuation.

160 diovascular disease (ASCVD) and are prone to statin-related adverse events from drug-drug interaction

161 objective muscular AEs relative to all other statins (reporting odds ratio, 1.53 [95% CI, 1.49-1.58])

162 hypertensive drugs, anti-platelet agents and statins) seem to have little or no effect on CKD-associa

163 cholesterol synthesis, which correlated with statin sensitivity across NBL cell lines, thus providing

164 Statin sensitivity was driven by HMGCR expression, the r

165 Consistently, PDACs in patients receiving statins show enhanced mesenchymal features.

166 rs of membrane trafficking they may underlie statin specific pleiotropic effects.

167 Nsdhl or treatment with cholesterol-lowering statins switches glandular pancreatic carcinomas to a ba

168 , since they are high-value intermediates in statin synthesis.

169 Medical prevention with antithrombotic and statin therapies is a mainstay of treatment to prevent a

170 tes mellitus (OR, 0.93 [95% CI, 0.74-1.19]), statin therapy (OR, 0.88 [95% CI, 0.68-1.14]), or cardia

171 ical therapy (SMT) with no LDL apheresis and statin therapy alone.

172 Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversif

173 ted LDL cholesterol levels despite receiving statin therapy at the maximum tolerated dose.

174 identified fewer younger adults eligible for statin therapy at the time of their MI than the 2013 gui

175 et a guideline indication for high-intensity statin therapy based on the PCE versus only 10% to 15% u

176 Asymptomatic subjects eligible for statin therapy by risk score were enrolled in a prospect

177 Adding ezetimibe to statin therapy did not increase discontinuation risk.

178 Statin therapy eligibility was determined using the 2013

179 Data are limited regarding statin therapy for primary prevention of atherosclerotic

180 deration of initiation or intensification of statin therapy for primary prevention to mitigate the in

181 ddition of evolocumab to maximally tolerated statin therapy had no impact on patient-reported cogniti

182 Patients with elevated triglycerides despite statin therapy have increased risk for ischemic events,

183 y prevention patients may be recommended for statin therapy if high CAD PRS were considered a guideli

184 d to more definitively determine the role of statin therapy in older adults for primary prevention of

185 ating that additional clinical evaluation of statin therapy in patients on dialysis undergoing arteri

186 ASCVD risk-reduction interventions including statin therapy in patients with PAD are warranted.

187 Here we assess the potential effect of statin therapy on cancer risk using evidence from human

188 ional risk factors to evaluate the effect of statin therapy on cardiovascular events.

189 then assessed longitudinally the effects of statin therapy on primary murine fistula patency and mat

190 orrespond with increased recommendations for statin therapy per the American College of Cardiology/Am

191 uation of statins is advised, but initiating statin therapy to treat COVID-19 is as yet unsubstantiat

192 after ACS, 18,924 patients on high-intensity statin therapy were randomized to alirocumab or placebo

193 servational and randomised studies comparing statin therapy with control (placebo or no treatment) in

194 a recent acute coronary syndrome on optimal statin therapy, alirocumab improves cardiovascular outco

195 d atherogenic lipoproteins despite intensive statin therapy, alirocumab was associated with large abs

196 atherogenic lipoproteins, despite intensive statin therapy, targeting LDL-C levels of 25 to 50 mg/dL

197 enic and inflammatory macrophage response to statin therapy, using the fibrin-targeted, near-infrared

198 were on high-intensity or maximum-tolerated statin therapy, with a baseline low-density lipoprotein

199 re likely to benefit from primary prevention statin therapy.

200 s, potentially impacting guideline-indicated statin therapy.

201 Secondary analysis was performed based on statin therapy.

202 a recent acute coronary syndrome on optimal statin therapy.

203 n in patients with (60%) or without baseline statin therapy.

204 ended statin eligibility and higher rates of statin therapy.

205 n in patients already receiving maximum-dose statin therapy.

206 sterol >=100 mg/dL despite maximum tolerated statin therapy.

207 in dyslipidemic PLHIV on maximally-tolerated statin therapy.

208 high-density cholesterol >=100 mg/dl despite statin therapy.

209 ixed dyslipidemia taking maximally-tolerated statin therapy.

210 hyl-glutaryl-coenzyme A reductase inhibitor (statin) therapy than middle-aged and older adults.

211 We established that statin, through inhibition of the mevalonate pathway, ca

212 geting one of these pathways synergizes with statins to produce a robust antitumor response.See relat

213 ew the mechanisms and clinical importance of statin toxicity and focus on the evaluation and manageme

214 0.02%CVC(max) /%(baseline) ; P = 0.024) and statin-treated (0.12 +/- 0.05%CVC(max) /%(baseline) ; P

215 2020) comparing omega-3 CA with corn oil in statin-treated participants with high cardiovascular ris

216 Among statin-treated patients at high cardiovascular risk, the

217 placebo-controlled trial, randomly assigned statin-treated patients with elevated triglycerides (135

218 nd subsequent coronary revascularizations in statin-treated patients with elevated triglycerides and

219 REDUCE-IT randomized 8179 statin-treated patients with qualifying triglycerides >=

220 In statin-treated patients with recent acute coronary syndr

221 c events; however, the cost-effectiveness in statin-treated patients with recent acute coronary syndr

222 ferent for statin (0.82 [0.73-0.91]) and non-statin treatment (0.67 [0.47-0.95]; p(interaction)=0.64)

223 They also inform the pharmacogenetics of statin treatment by demonstrating that benefit from rosu

224 00-1.14) received lower absolute benefits of statin treatment compared with males (LHH range: 2.55-3.

225 t more than 90% of patients who discontinued statin treatment could be rechallenged with the same or

226 s cholesterol as a proviral factor, although statin treatment did not show antiviral efficacy in pati

227 Compared with statin treatment discontinuation, nondaily statin dosing

228 Statin treatment eligibility was determined by predicted

229 Statin treatment equally inhibited Rac1 inhibition in pr

230 duction and T2D incidence increases across 3 statin treatment guidelines or recommendations among adu

231 iation between end-points and high-intensity statin treatment in TIA patients with positive and negat

232 istory of ASCVD or T2D who were eligible for statin treatment initiation.

233 tor, providing a new mechanism through which statin treatment may impact PDAC growth.See related arti

234 High-dose statin treatment seems to reduce cardiovascular complica

235 Even with statin treatment to lower LDL cholesterol, patients with

236 y syndrome on intensive or maximum-tolerated statin treatment who were randomized to the PCSK9 inhibi

237 ate the increased oxidative stress caused by statin treatment, and targeting one of these pathways sy

238 e of lipid-lowering therapies, including non-statin treatment, in older patients.

239 iota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence

240 GCR gene region, which represent proxies for statin treatment, were associated with overall cancer ri

241 d atherogenic lipoproteins despite optimized statin treatment.

242 yl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment for dyslipidemia, and group 2, those w

243 ns based on shorter-term effects observed in statin trials (model A) and longer-term benefits based o

244 2 diabetes (T2D), evidence has emerged from statin trials and candidate gene investigations suggesti

245 t 75 years, of whom 11 750 (54.7%) were from statin trials, 6209 (28.9%) from ezetimibe trials, and 3

246 Chronic statin usage is protective against post ERCP pancreatiti

247 Statin usage was found to be protective against PEP, (OR

248 ng participants with dyslipidemia even under statin usage.

249 erminant of noncalcified plaque progression, statin use (beta=-2.178; P=0.050) was borderline signifi

250 diabetes mellitus (beta=1.725; P=0.012), and statin use (beta=1.498; P=0.046) showed an independent a

251 OR, 2.03; 95% CI, 1.20-3.46; P = 0.008), and statin use (OR, 1.98; 95% CI, 1.07-3.66; P = 0.029) than

252 nfluenza illness was not affected by current statin use among persons aged >=45 years.

253 Interactions were sought between statin use and dementia risk factors.

254 ther studies are needed to determine whether statin use and/or dyslipidemia increases the risk of DED

255 ervention, concomitant disease presence, and statin use did not show statistical significance.

256 Dyslipidemia and statin use have been associated with colorectal cancer (

257 e mechanisms underlying clinical outcomes of statin use in patients.

258 The potential benefits of statin use in PWH with normal lipid levels requires furt

259 community-dwelling adults >=70 years of age, statin use may be beneficial for preventing physical dis

260 s the impact of clinical characteristics and statin use on quantitatively assessed coronary plaque pr

261 We aimed to determine the effect of statin use on the risk of cancer development and surviva

262 A history of statin use or dyslipidemia is associated with an increas

263 ratified by percent stent use and by percent statin use to evaluate outcomes in contemporary trials.

264 Conclusions Statin use was associated with an increased progression

265 Statin use was associated with significantly reduced ris

266 Statin use was common before (40%) and during admission

267 Statin use was lower in patients with PAD only (33.9%) v

268 dian follow-up period of 4.7 years, baseline statin use was not associated with disability-free survi

269 and older and free of ASCVD at baseline, new statin use was significantly associated with a lower ris

270 sence of low-, moderate-, and high-intensity statin use were 1.39 (95% confidence interval [CI]: 1.13

271 and statin intolerance/contraindications to statin use were present in 20.7% of patients.

272 dels were fit to evaluate the association of statin use with outcomes.

273 g, hemoglobin A1c <=9% in diabetic patients, statin use, and antiplatelet use-termed optimal medial t

274 sure, diastolic blood pressure, tobacco use, statin use, body mass index, urine microalbumin-to-creat

275 On univariate analysis, young age, no statin use, history of PEP, and endoscopic sphincterotom

276 Statin use, overall, was a non-significant protective fa

277 AMD remained after adjustment for history of statin use, smoking status, body mass index, and history

278 ign was used, excluding those with any prior statin use.

279 se changes were independent of CVRF, age and statin use.

280 variable analysis provided weak evidence for statin use.

281 wer risk for major amputation included prior statin use.

282 ients with cirrhosis despite data supporting statin use. We investigated the independent effects of h

283 ns and lower mortality (1.8% vs 2.3% without statin use; P < .001) in observational studies, and shou

284 ence interval [CI]: 21.6 to 22.3) in current statin users and 30.1 (95% CI: 30.2 to 30.6) in former u

285 o difference in brain volume changes between statin users and never users.

286 We compared influenza VE in statin users and nonusers aged >=45 years enrolled in th

287 nd 98.2 total deaths/1000 person-years among statin users and nonusers, respectively (weighted incide

288 ovascular deaths per 1000 person-years among statin users and nonusers, respectively (weighted IRD/10

289 66.3 and 70.4 events/1000 person-years among statin users and nonusers, respectively (weighted IRD/10

290 9, A(H3N2), and B viruses were similar among statin users and nonusers.

291 The number of statin users in cases and controls was 73 (19%) and 403

292 r a composite of ASCVD events when comparing statin users with nonusers.

293 nts with PAD were less likely to be taking a statin versus those with CHD or cerebrovascular disease.

294 y (ILLT) comprising single LDL apheresis and statins versus standard medical therapy (SMT) with no LD

295 atment of patients with estrogen, metformin, statins, vitamin D, and tumor necrosis factor blockers a

296 7 U.S. Food and Drug Administration-approved statins, we examined pitavastatin as a drug candidate fo

297 of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates

298 95%CI: 0.70-1.01, p = 0.060), but lipophilic statins were associated with a CRC risk reduction (OR 0.

299 Statins, which are frequently prescribed for patients wi

300 these trials have established the safety of statins with regard to nonvascular mortality and cancer.