ライフサイエンスコーパス: liver injury

1 hophysiological diversity of human alcoholic liver injury.

2 gy balance, but excess BAs cause cholestatic liver injury.

3 creases in total bilirubin or other signs of liver injury.

4 is relatively weak exacerbated steatosis and liver injury.

5 der age and hepatitis B positivity predicted liver injury.

6 pha regulation of Ctgf post-various types of liver injury.

7 and protected mice from CCl(4)-induced acute liver injury.

8 OS/NO signaling module is interrupted during liver injury.

9 or signaling in a mouse model of cholestatic liver injury.

10 ne cells are also implicated in APAP-induced liver injury.

11 and engraftment of bone marrow sprocs after liver injury.

12 s inversely correlated with the surrogate of liver injury.

13 tigated APAP-induced hepatocyte necrosis and liver injury.

14 g plays a pathogenic role in alcohol-induced liver injury.

15 ransport as therapy for macrophage-dependent liver injury.

16 peutic target for patients with drug-induced liver injury.

17 hepcidin and iron homeostasis regulation and liver injury.

18 st, or cause susceptibility to, APAP-induced liver injury.

19 and subsequent pathological changes of acute liver injury.

20 ehydes, steatosis, ER stress, apoptosis, and liver injury.

21 d novel therapeutic targets for APAP-induced liver injury.

22 Lieber DeCarli diet causing ethanol-induced liver injury.

23 arance of HBV-infected cells causing limited liver injury.

24 e impact of HMGCR repression in TCDD-induced liver injury.

25 an anti-CCL2 mAb attenuated the severity of liver injury.

26 more significantly to the pathology of acute liver injury.

27 promising therapeutic agent for APAP-induced liver injury.

28 th antibody-drug conjugates (ADCs) may cause liver injury.

29 are a major source of new hepatocytes after liver injury.

30 orylation is mainly involved in APAP-induced liver injury.

31 revented VPA- and APAP-induced ER stress and liver injury.

32 or of macrophage function after APAP-induced liver injury.

33 alis(5,6)-as a cause of hepatocyte death and liver injury.

34 antiviral T cell responses and ameliorating liver injury.

35 nction predisposing patients to drug-induced liver injury.

36 nd CIDEA is related to NAFLD progression and liver injury.

37 There is a dearth of studies on NHPs induced liver injury.

38 vated TNF-alpha level confirmed incidence of liver injury.

39 n of cell death in autoimmune-mediated acute liver injury.

40 failure to adapt, with progression to overt liver injury.

41 r of liver tissue repair following localized liver injury.

42 correlated with the NAFLD activity score and liver injury.

43 disease, such as silicosis and drug-induced liver injury.

44 d indicate 20% as a threshold of more severe liver injury.

45 s NR may be therapeutic in settings of acute liver injury.

46 Autophagy has a protective effect on acute liver injury.

47 hepatic stellate cells (HSCs) during chronic liver injury.

48 dothelin-1 and CAV1 scaffolding domain after liver injury.

49 exposure to PFAS can contribute to pediatric liver injury.

50 collagen content, and noninvasive markers of liver injury.

51 issue slices, and mice with acute-on-chronic liver injury.

52 athogenic properties of IL-22 during chronic liver injury.

53 sts will miss most patients with significant liver injury.

54 egulates infection response and increases in liver injury.

55 R chaperones, and (3) greater cell death and liver injury.

56 evere, chronic liver disease or drug-induced liver injury.

57 matory cytokines involved in alcohol-induced liver injury.

58 ted by AST, correspond with COVID-19-related liver injury.

59 -responsive T-cell clones from patients with liver injury.

60 manipulated for therapeutic benefit in acute liver injury.

61 AR inhibitors to ameliorate alcohol-induced liver injury.

62 stant to alcohol-induced adipose atrophy and liver injury.

63 tress and inflammation in macrophages during liver injury.

64 critical for tissue protection during acute liver injury.

65 ed etiology or an unrelated and coincidental liver injury.

66 phic or comorbid illness was associated with liver injury.

67 etuates and worsens liver damage after toxic liver injury.

68 ions, focusing on idiosyncratic drug-induced liver injury.

69 mitted to the clinic with symptoms of severe liver injury.

70 cardiovascular, renal, gastrointestinal and liver injuries.

71 egulating a long noncoding RNA DINO in acute liver injuries.

72 liferation of reactive bile ducts induced by liver injuries.

73 ty factor to drug- or toxicant-induced acute liver injuries.

74 Inactivation of the APR can promote liver injury, a frequently observed organ dysfunction du

75 secreted into the extracellular matrix upon liver injury, acting as a cytokine stimulates the deposi

76 Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contri

77 Acute liver injury after any insult, including APAP overdose,

78 mportantly, Areg(-/-) mice showed aggravated liver injury after BDL and ANIT administration compared

79 ing intestinal TLR9 had profoundly increased liver injury after hepatic IR compared to WT mice with e

80 However, CD160(-/-) mice exhibit severe liver injury after in vivo challenge with alpha-galactos

81 a(mye/-) ) markedly exacerbated APAP-induced liver injury (AILI) without affecting APAP bioactivation

82 crosis plays a critical role in APAP-induced liver injury (AILI).

83 In a mouse model of ALD, liver injury (alanine aminotransferase [ALT]) and steato

84 19 (COVID-19) has been associated with acute liver injury (ALI) manifested by increased liver enzymes

85 olled consecutive patients with ALF or acute liver injury (ALI; INR >= 2.0 with no encephalopathy), o

86 Markers of cholestasis and liver injury, alkaline phosphatase (ALP), and total and

87 f normal [ULN]) in 22.2% (n = 18) and severe liver injury (ALT > 5x ULN) in 12.3% (n = 10).

88 ferase (ALT) during COVID-19 showed moderate liver injury (ALT 2-5x upper limit of normal [ULN]) in 2

89 hological features were that of drug induced liver injury, although an abnormal amount of copper was

90 High incidence rates of liver injury among cotreated human immunodeficiency viru

91 s trial demonstrates high incidence rates of liver injury among human immunodeficiency virus (HIV)-tu

92 PTB is successfully reproduced in mice with liver injuries and dysregulated bile acids.

93 ceptibility to high cholesterol diet-induced liver injury and abolished the protective effect against

94 ow sproc recruitment, and thereby ameliorate liver injury and accelerate liver regeneration, whereas

95 injury (DILI) is an important cause of acute liver injury and accounts for approximately 10% of all c

96 ociates with established serum biomarkers of liver injury and alterations in serum metabolome in chil

97 Prevalence of liver injury and associated clinical characteristics are

98 tic lipid distribution and metabolism during liver injury and confirm nonlinear multimodal imaging as

99 are frequently used to investigate alcoholic liver injury and define new therapeutic targets.

100 -ILE alone while still preventing PN-induced liver injury and EFAD in mice.

101 We have shown that liver injury and Ehrlichia-induced sepsis occur due to d

102 Currently, liver injury and failure are observed in up to 20% of pa

103 The frequency of acquired liver injury and failure in critical illness has been si

104 for the evaluation and treatment of acquired liver injury and failure in critically ill patients.

105 agnostic and therapeutic options of acquired liver injury and failure.

106 us preventing the development of cholestatic liver injury and fibrosis after bile duct ligation (BDL)

107 matosis models, Smad158;Alb-Cre(+) developed liver injury and fibrosis at 8 weeks.

108 NAC reduced liver injury and fibrosis in mice with biliary atresia,

109 (a predominant form in the liver) attenuated liver injury and fibrosis in the HFD(+Cxcl1) -induced NA

110 w that Klf10 deficient mice display enhanced liver injury and fibrosis priming upon MCDD challenge.

111 Using AQP3 knockout mice in a model of liver injury and fibrosis produced by CCl(4), we obtaine

112 a model of hemochromatosis that encompasses liver injury and fibrosis seen in human disease.

113 Cholestatic liver injury and fibrosis were assessed by serum biochem

114 Liver injury and fibrosis were prevented in Smad158;Alb-

115 oth iron loading and SMAD1/5/8 deficiency in liver injury and fibrosis.

116 (NIK) is a key trigger in the development of liver injury and fibrosis.

117 e cell recruitment and ultimately influences liver injury and fibrotic tissue remodelling in the Mdr2

118 mitigated both LPS/D-Galn- and ConA-induced liver injury and immune hyperactivation, whereas exogeno

119 e expression in several models of periportal liver injury and impairs liver regeneration, leading to

120 r I], and interleukin-6), YKL-40 (related to liver injury and inflammation), 2 biomarkers related to

121 Its overuse provokes liver injury and it is the second most common cause of l

122 coprotein resides at the interface of immune liver injury and metabolic homeostasis, its role in orth

123 eagues on the association between markers of liver injury and mortality in coronavirus disease 2019 (

124 dynamicity correlated with COVID-19-related liver injury and patient outcomes.

125 bile acid sequestrant sevelamer reversed the liver injury and prevented the progression of NASH, incl

126 ant AREG protected from ANIT and BDL-induced liver injury and reduced BA-triggered apoptosis in liver

127 iver in several clinical settings, including liver injury and regeneration after major surgery and pr

128 by a family of growth factors induced during liver injury and regeneration.

129 and, amphiregulin (AREG), during cholestatic liver injury and regulation of AREG expression by BAs.

130 cued FXR signaling and partially ameliorated liver injury and sinusoidal ischemia in SCD mice.

131 Despite LD mice have increased liver injury and steatosis by alcohol exposure, the numb

132 improvement in liver function and markers of liver injury and the positive effects of reversal of ins

133 as they transition to myofibroblasts during liver injury and the wound healing response.

134 tment outcomes in acute kidney injury, acute liver injury and wound healing.

135 ization, colitis, and potential drug-induced liver injury) and one of four patients had adverse event

136 tendon disorder, and potential drug-induced liver injury) and one of four patients had adverse event

137 R inhibition remarkably decreased steatosis, liver injury, and fibrosis and improved glucose toleranc

138 ty state on hepatic steatosis, inflammation, liver injury, and fibrosis during the transition of NAFL

139 iving the pathogenesis of APAP-induced acute liver injury, and PLD2 may therefore represent an import

140 licate the involvement of macrophage AQP3 in liver injury, and provide evidence for mAb inhibition of

141 ng energy intake, energy disposal, lipotoxic liver injury, and the resulting inflammation and fibroge

142 HS, RvD1 attenuated the kidney dysfunction, liver injury, and tissue ischemia.

143 ificantly induced in patients with alcoholic liver injury, and was co-localized with alphaSMA-express

144 ing enhances liver recovery from acute toxic liver injuries (APAP and carbon tetrachloride) by increa

145 the mechanisms of APAP-induced necrosis and liver injury are not fully understood.

146 TSP-1(-/-) mice administered AOM had reduced liver injury as assessed by histology and serum transami

147 on protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standa

148 patients with anti-tuberculosis drug induced liver injury (AT-DILI).

149 In two murine models of cholestatic liver injury, bile duct ligation (BDL) and alpha-naphthy

150 t was associated with transient elevation of liver injury biomarkers and enhanced proliferative respo

151 e that is up-regulated by hepatocytes during liver injury but is expressed at significantly lower lev

152 s disease 2019 (COVID-19) is associated with liver injury, but the prevalence and patterns of liver i

153 n monoxide ameliorates acetaminophen-induced liver injury by increasing hepatic HO-1 and Parkin expre

154 an extracellular epitope on AQP3, prevented liver injury by inhibition of AQP3-mediated H(2)O(2) tra

155 es plays a crucial role to prevent excessive liver injury by regulating the induction of cell death a

156 caused stellate cell activation, leading to liver injury, by a mechanism involving AQP3-mediated H(2

157 The liver injury can present with a hepatocellular, cholesta

158 Conclusion: Chronic liver injury can recruit BM progenitors of LSECs that en

159 Drug-induced liver injury caused by acetaminophen (acetyl-para-aminop

160 t a therapeutic target to prevent and rescue liver injury caused by acetaminophen.

161 -dihydroxy-5b-cholan-24-ol rescues mice from liver injury caused by APAP.

162 non-HLA variant that associates with risk of liver injury caused by multiple drugs and validated our

163 New onset or worsening drug-induced liver injury challenges coinfected patients on antiretro

164 as different forms of cutaneous eruptions or liver injury consistent with priming of an immune respon

165 ease and a mouse model of chemically induced liver injury despite marked activation and spontaneous I

166 ers are suboptimal in detecting drug-induced liver injury (DILI) and predicting its outcome.

167 Drug-induced liver injury (DILI) developed in 26 (7.9%) InO recipient

168 Patients with drug-induced liver injury (DILI) frequently have comorbid conditions,

169 g discovery and development and drug-induced liver injury (DILI) is a leading cause of preclinical an

170 Drug-induced liver injury (DILI) is a leading cause of termination in

171 Drug induced liver injury (DILI) is a necro-inflammatory liver diseas

172 Drug-induced liver injury (DILI) is a patient-specific, temporal, mul

173 Idiosyncratic drug-induced liver injury (DILI) is a rare, often difficult-to-predic

174 Drug-induced liver injury (DILI) is an adverse reaction to drugs or o

175 Drug induced liver injury (DILI) is an important cause of acute liver

176 Drug-induced liver injury (DILI) is an important cause of death and i

177 Drug-induced liver injury (DILI) is the leading cause of liver failur

178 of patients with idiosyncratic drug-induced liver injury (DILI) to identify variants associated with

179 specific microRNA biomarker for drug-induced liver injury (DILI).

180 o drug safety concerns, such as drug-induced liver injury (DILI).

181 TBs are at an increased risk of drug-induced liver injury (DILI).

182 lthy mice, which was associated with reduced liver injury, diminished proliferation of hepatocytes an

183 HSCs play an essential role in ConA-induced liver injury directly via the interferon-beta/IRF1 axis,

184 knockout (KO) mice exhibited far more severe liver injuries due to impaired DINO induction and p53 ac

185 nile mice developing progressive cholestatic liver injury due to impaired biliary phosphatidylcholine

186 toxicity with limited evidence of benefit in liver injury due to other causes.

187 Liver injury during COVID-19 was significantly associate

188 comes, maternal TB, all-cause mortality, and liver injury during pregnancy through 12 months postpart

189 All cases of drug-induced liver injury enrolled into a prospective database over a

190 NAFLD) represents a growing cause of chronic liver injury, especially in western countries, where it

191 and Tr(-/-)Mdr2(-/-) mice were assessed for liver injury, fibrosis, and ductular reactive (DR) cells

192 sustained inflammatory response that promote liver injury, fibrosis, cirrhosis, and oncogenic transfo

193 isruption of Hif1alpha developed less-severe liver injury following administration of ethanol, inject

194 agonist pioglitazone on tumor metastasis and liver injury following IRI in a mouse model of colon can

195 te, and sequential arms) developed new-onset liver injury following TB treatment initiation.

196 afe in selected patients at very low risk of liver injury from acetaminophen overdose.

197 Recent findings that autophagy blocks mouse liver injury from lipopolysaccharide led to an examinati

198 l and autoimmune hepatitis, and drug-induced liver injury from prescription drugs, and herbal and die

199 During the pathological progress of acute liver injury, GSH levels are decreased, and this is sign

200 This coupled with the fact that liver injury had a delayed onset suggests that the adapt

201 A role of FXR in drug-induced liver injury has also been hypothesized yet only margina

202 Liver injury has been reported as a nonpulmonary manifes

203 Two types of drug induced liver injury have been recognized: intrinsic and idiosyn

204 nusoidal ischemia, progressive hepatomegaly, liver injury, hyperbilirubinemia, and increased ductular

205 94 administration markedly blocked the acute liver injury in a dose-dependent manner, showing almost

206 investigate the consequences of early septic liver injury in a murine model of polymicrobial abdomina

207 Predicting drug-induced liver injury in a preclinical setting remains challengin

208 ozygous mutation in kdsr induced predisposed liver injury in adult zebrafish.

209 induced steatosis, ER stress, apoptosis, and liver injury in both experimental and human ALD.

210 Secondary forms of liver injury in critical illness are divided primarily i

211 2)O(2) and glycerol transport, and prevented liver injury in experimental animal models.

212 ctin, or the complement system could prevent liver injury in hemolytic diseases like sickle cell dise

213 y can accurately measure miR-122 to diagnose liver injury in humans and other species and can overcom

214 c PDE4 and cAMP levels play a causal role in liver injury in in vivo and in vitro models of ALD.

215 r injury, but the prevalence and patterns of liver injury in liver transplantation (LT) recipients wi

216 Variables associated with liver injury in LT recipients were younger age (P = 0.00

217 ased hepatic AHR-battery gene expression and liver injury in male, but not female, mice.

218 Liver injury in mice and humans increases levels of YAP/

219 VLX103 effectively decreases toxin-induced liver injury in mice and may be an effective therapy for

220 ed at 808 nm, enabling label-free imaging of liver injury in mice and the discrimination of pathologi

221 egeneration after carbon tetrachloride toxic liver injury in mice with conditional deletion of Yap/Ta

222 e atrophy, which ameliorates alcohol-induced liver injury in mice.

223 d preserve the ability to prevent PN-induced liver injury in mice.

224 against APAP-induced hepatocyte necrosis and liver injury in mice.

225 and patients with PBC, promoting BA-induced liver injury in part by targeting MLL4.

226 The DCL assay also identified liver injury in rats and dogs.

227 of bile acids in the liver, fails to promote liver injury in the absence of the microbiome in vivo.

228 ons, with indicators of cellular stress with liver injury in the human hepatic HepaRG cell line, and

229 How IL-1beta promotes liver injury in these diseases is unclear, as no IL-1bet

230 etely prevented development of steatosis and liver injury in this model.

231 c role of PDGFR-alpha in HSCs during chronic liver injury in vivo via regulation of HSC survival and

232 etylcysteine (NAC) treatment of APAP-induced liver injury in wild-type mice, the liver injury of NR2E

233 Acute CCl4 -mediated liver injury in WT mice induced endogenous CcnE1 express

234 rom simple steatosis to more severe forms of liver injury including nonalcoholic steatohepatitis (NAS

235 They concluded that the dynamic patterns of liver injury indicators, represented by AST, correspond

236 Chronic alcohol consumption causes liver injury, inflammation and fibrosis, thereby increas

237 Liver injury is a common complication of first-line anti

238 Chronic liver injury is a risk factor for cirrhosis and hepatoce

239 Liver injury is associated with higher mortality and ICU

240 Liver regeneration after APAP-induced liver injury is dose dependent and impaired after severe

241 ogical interactions pathway in patients with liver injury is indicative of an immune-based mechanism

242 Gpbar1 gene deletion worsens the severity of liver injury, its pharmacological activation by 6beta-et

243 NK phosphorylation in the APAP-induced acute liver injury model.

244 d polyploid hepatocytes in several different liver injury models and found robust proliferation in al

245 Here we explore the role of KLF6 in acute liver injury models in mice, and in patients with acute

246 Using a variety of genetic, metabolic, and liver injury models in mice, we manipulated Hippo signal

247 riptional analyses in two independent murine liver injury models, we discover adaptive reprogramming

248 sms of liver regeneration after APAP-induced liver injury, more comprehensive research in this area i

249 or 306 patients enrolled in the Drug-Induced Liver Injury Network prospective study at Indiana Univer

250 We analyzed patients in the US Drug-Induced Liver Injury Network prospective study having a fatal ou

251 No patients represented with liver injury, none died, and 96 of 96 were well at 14-da

252 APAP)- or carbon tetrachloride-induced acute liver injuries, NR2E3 knockout (KO) mice exhibited far m

253 Severe and life-threatening liver injury occurred in 2, 7, and 3 early, late, and se

254 tified a profile of children at high risk of liver injury (odds ratio, 1.56; 95% confidence interval,

255 -induced liver injury in wild-type mice, the liver injury of NR2E3 KO mice was not effectively revers

256 nine aminotransferase (ALT) for drug-induced liver injury often assume that the biomarker is released

257 hways could differ depending on the specific liver injury or animal models used in the study.

258 There were no cases of drug-induced liver injury or clinically relevant hepatic decompensati

259 e proliferation and hepatomegaly without any liver injury or tissue loss.

260 ere damage such as cardiovascular, renal and liver injury or/and multiple organ failure, suggesting a

261 n, this congestive condition led to an acute liver injury overlapping pre-existing hepatic fibrosis.

262 osuppression (49.4%) was not associated with liver injury (P = 0.156) or mortality (P = 0.084).

263 combined a mouse model of acute cholestatic liver injury, partial bile duct ligation (pBDL), with a

264 , and advanced disease, and serum markers of liver injury, particularly bilirubin and ALP, are used t

265 difference was observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a signific

266 The incidence of liver injury post-ART initiation in patients with CD4+ c

267 During liver injury, quiescent hepatic stellate cells (qHSCs) t

268 t common liver disease occur by two steps of liver injury ranges from steatosis to nonalcoholic steat

269 After liver injury, regeneration occurs through self-replicati

270 yte autophagy contributes to alcohol-induced liver injury remain unclear.

271 s were tracked with bone marrow recovery and liver injury, respectively, providing proof-of-concept v

272 e from an index case of atabecestat-mediated liver injury revealed an infiltration of T-lymphocytes i

273 rentiation; however, its function in chronic liver injury sequelae, such as fibrosis, is unknown.

274 sed subjects retrospectively for cardiac and liver injury, shock, ventilation, mortality, and viral c

275 before the start of treatment, drug-induced liver injury should be taken into consideration, especia

276 45% had mild, 21% moderate, and 6.4% severe liver injury (SLI).

277 sion, given that it paves the way for severe liver injuries such as fibrosis and cirrhosis.

278 del, we show that CB caused lower degrees of liver injury than pure EtOH by protecting against the de

279 P-9 inhibition may be a therapeutic tool for liver injury that damages the vasculature, whereas syste

280 e of functional compensation following acute liver injury that occurs prior to cellular proliferation

281 ut) animals, which were subjected to chronic liver injury through carbon tetrachloride treatment, bil

282 ed hepatocytes to lipopolysaccharide-induced liver injury (TNF-alpha, ALT, and lactate dehydrogenase

283 ms to impair hepatocyte proliferation during liver injury to evaluate the contribution of non-hepatoc

284 drogel carriers in a rodent model of chronic liver injury to highlight the potential translational ut

285 (PLD2) on acetaminophen (APAP)-induced acute liver injury using a PLD2 inhibitor (CAY10594).

286 regulate hepatocyte repopulation after toxic liver injury using fumarylacetoacetate hydrolase-deficie

287 tate hydrolase-deficient mice at the time of liver injury via hydrodynamic tail-vein injection.

288 Chronic liver injury was induced in BoyJ mice by injection of ca

289 e and COVID-19 (n = 375), incidence of acute liver injury was lower in LT recipients (47.5% vs. 34.6%

290 Liver injury was observed in RelA-null (hepRelA(Delta/De

291 In studies of mice with chronic liver injury, we showed the antifibrotic effects of repe

292 led that patients with a high viral load and liver injury were more likely than other patients to spr

293 pups were rendered resistant to RRV-mediated liver injury when Ly6c(Lo) non-classical monocytes were

294 Compared with the liver injury, which is established before most patients

295 inal failure (CIF) often develop cholestatic liver injury, which may lead to liver failure and need f

296 nfants describes repeated episodes of severe liver injury with recovery of hepatic function between c

297 liver to LPS-induced lipid accumulation and liver injury with significantly increased hepatic steato

298 nd protected Mdr2(-/-) mice from spontaneous liver injury, with improved liver enzymes, inflammation,

299 te cells (aHSCs) orchestrate scarring during liver injury, with putative quiescent precursor mesoderm

300 tion of normal hepatocyte architecture after liver injury, with resultant fibrosis.