ライフサイエンスコーパス: liver injury

1 fibrosis) or acetaminophen (to induce toxic liver injury).

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

3 esized that IL-22BP may play a role in acute liver injury.

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

5 onfirmed in mice with concanavalin A-induced liver injury.

6 s study was to elucidate the role of PTX3 in liver injury.

7 were the main cell types expressing PTX3 in liver injury.

8 sed repeatedly into mice undergoing fibrotic liver injury.

9 ed increased hepatic fibrosis in response to liver injury.

10 nce was T cell dependent and associated with liver injury.

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

12 oluble B7 compared to sera from mice without liver injury.

13 lation of cholesterol synthesis that affects liver injury.

14 mouse model and examined TnC expression and liver injury.

15 IgA and IgA deposits in liver and prevented liver injury.

16 cient mice, were protected from ConA-induced liver injury.

17 ecause of the high frequency of drug-induced liver injury.

18 osis induced by hepatotoxins that results in liver injury.

19 he innate immune system, further aggravating liver injury.

20 rather than just JNK1, in the onset of toxic liver injury.

21 rosis in an experimental setting of chemical liver injury.

22 increased porphyrin accumulation, and marked liver injury.

23 ng mice from CCl4- and acetaminophen-induced liver injury.

24 elays tumor development in mice with chronic liver injury.

25 regarded as a T cell-mediated model of acute liver injury.

26 ssociation is affected by factors other than liver injury.

27 ential therapeutic target in immune-mediated liver injury.

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

29 cumented, clinically apparent, idiosyncratic liver injury.

30 crophage infiltration without an increase in liver injury.

31 Dysregulation of liver metabolism may cause liver injury.

32 e resistant to Concanavalin A (ConA)-induced liver injury.

33 activation of NKT cells during ConA-induced liver injury.

34 thy volunteers and patients with less severe liver injury.

35 collagen content, and noninvasive markers of liver injury.

36 than C57BL/6 and FVB/N mice to Fas-mediated liver injury.

37 otentially targeted to alleviate cholestatic liver injury.

38 TnC in obese patients with various levels of liver injury.

39 r model to investigate acetaminophen-induced liver injury.

40 nctions early post-APAP, thereby aggravating liver injury.

41 been reported to block acetaminophen-induced liver injury.

42 otected Jnk(Deltahepa) and control mice from liver injury.

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

44 ents for assessing causality in drug-induced liver injury.

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

46 essential to predict unexpected drug-related liver injury.

47 rs to be anti-fibrotic and protective during liver injury.

48 ce, or Mdr2(-/-) mouse models of cholestatic liver injury.

49 s a novel therapeutic target for cholestatic liver injury.

50 ter partial hepatectomy and acute or chronic liver injury.

51 1 expression in rodent models of cholestatic liver injury.

52 ine and choline-deficient (MCD) diet-induced liver injury.

53 and necrosis are markers of ethanol-induced liver injury.

54 re important to the development of alcoholic liver injury.

55 tection against alcohol- or MCD diet-induced liver injury.

56 lates inflammasome activation in cholestatic liver injury.

57 aintain liver homeostasis during BDL-induced liver injury.

58 sts will miss most patients with significant liver injury.

59 els of alanine aminotransferase, a marker of liver injury.

60 present Kupffer cell studies in cholestatic liver injury.

61 were considerably resistant to ConA-induced liver injury.

62 cules in exacerbated cell death in steatotic liver injury.

63 ted B-cell abnormalities in a mouse model of liver injury.

64 NA cargo, which are specific for ASH-related liver injury.

65 Autophagy has a protective effect on acute liver injury.

66 tive hepatocyte death to investigate sterile liver injury.

67 fore investigated their role in ConA-induced liver injury.

68 sickness behaviors in mice with cholestatic liver injury.

69 s evident with progressive clinical signs of liver injury.

70 r fibrosis if applied after onset of chronic liver injury.

71 believed to occur during human drug-induced liver injury.

72 the prevention and treatment of hepatotoxic liver injury.

73 s not entirely critical to LPS-induced acute liver injury.

74 t liver regeneration after acute and chronic liver injuries.

75 vs 0, P = 0.03; 2 vascular, 2 splenic, and 1 liver injury; 1 reexploration to adjust graft positionin

76 uct loss were more likely to develop chronic liver injury (94% vs. 47%), which was usually cholestati

77 ubsequent inflammation, which can make acute liver injury a life-threatening event.

78 I IFNs, followed by hepatocyte apoptosis and liver injury, accompanied by liver fibrosis upon repeate

79 atment in children are to reduce severity of liver injury, achieve HBeAg seroconversion, and prevent

80 acologic stimulation of sirtuin 1 attenuates liver injury after hepatic ischemia-reperfusion by resto

81 RIP3 failed to protect and even exacerbated liver injury after mice were treated with lipopolysaccha

82 lthough mechanisms that trigger APAP-induced liver injury (AILI) are well known, those that halt the

83 duces monocyte infiltration and APAP-induced liver injury (AILI) in mice.

84 al normalised ratio (INR) characterise acute liver injury (ALI) and failure (ALF), yet a wide heterog

85 but it remains unclear if the risk of acute liver injury (ALI) is increased for statin initiators co

86 he safer approach since it does not increase liver injury, allows inflammation to take place but inhi

87 All serious liver injuries alter metabolism and initiate hepatic reg

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

89 ontribute to hepatitis C virus (HCV)-induced liver injury and are readily observed in Huh7.5 cells in

90 logs and attenuated viral infection-induced liver injury and body weight loss.

91 rious adverse events (potential drug-induced liver injury and depression or lipodystrophy) that led t

92 rategies aimed at halting the progression of liver injury and fibrogenesis in various liver pathogene

93 However, the HFC diet led to more severe liver injury and fibrosis compared to the HFD diet.

94 ing genetic risks and biological pathways to liver injury and fibrosis have led to a renewed interest

95 the M1 phenotype, thereby promoting chronic liver injury and fibrosis progression, but limiting angi

96 or methionine-choline-deficient (MCD) diet, liver injury and fibrosis were attenuated in Hrg(-/-) ,

97 identify potential novel strategies to treat liver injury and fibrosis, particularly as a consequence

98 ial effects of MSC therapy in the context of liver injury and fibrosis.

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

100 del to study the immune response to necrotic liver injury and found that necrotic liver cells induced

101 roles at every stage during the continuum of liver injury and healing.

102 ges shape the tissue microenvironment during liver injury and healing.

103 ates immune cells, resulting in inflammatory liver injury and hepatocyte necrosis.

104 ere cholestasis and had increased markers of liver injury and increased proliferation of biliary epit

105 ted against cholesterol accumulation-induced liver injury and inflammation in mice.

106 CC), which is associated with FoxO-dependent liver injury and inflammation.

107 d hepatocytes that regulates the response to liver injury and inflammation.

108 -healing response and attenuates LPS-induced liver injury and inflammation; therefore, administration

109 We describe a model of combined liver injury and inhibition of hepatocyte proliferation

110 HSCs are activated after liver injury and involved in pivotal processes, such as

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

112 of the biliary architecture that occurs upon liver injury and limit extracellular matrix deposition.

113 with Klebsiella pneumoniae, which results in liver injury and necrosis.

114 a high-fat diet for 12 weeks accelerated the liver injury and normalization of blood glucose levels.

115 Chronic inflammation leads to liver injury and progression of fibrosis.

116 nclusion, NOX4 is induced in early alcoholic liver injury and regulates CCR2/CCL2 mRNA stability ther

117 Mast cells (MCs) infiltrate following liver injury and release histamine, increasing biliary p

118 v/TM provided more potent protection against liver injury and release of pathological mediators than

119 ression was up-regulated in animal models of liver injury and strongly induced by lipopolysaccharide

120 ministration of lipopolysaccharide increased liver injury and the levels of peritoneal macrophage cyt

121 onstrated a proinflammatory phenotype during liver injury and the normal induction of Ly6C(lo) monocy

122 Strikingly, chronic liver injury and tumor development were markedly suppres

123 and sensitive microRNA (miRNA) biomarkers in liver injury and tumor progression could improve cancer

124 ty of MSCs to influence fibrotic response to liver injury and will explore the potential mechanisms t

125 GVHD clinical scores, reduced intestinal and liver injury, and decreased levels of serum and hepatic

126 ted with decreased IL-22 secretion, elevated liver injury, and impaired liver regeneration.

127 bonyl-1,4-dihydrocollidine models of chronic liver injury, and investigate the role of PDGFRalpha on

128 vers (HEALs), implanted them in mice without liver injury, and rapidly generated human liver chimeric

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

130 convert to an immature state during chronic liver injury, and we investigated whether this conversio

131 ostinjury inflammation in APAP-induced acute liver injury (APAP-ALI) and justifies development of ant

132 pharmacological inhibitor, MLN4924, reduced liver injury, apoptosis, inflammation, and fibrosis by t

133 As natural killer T cells and liver injury are central in liver regeneration, elucidat

134 ver, the majority of cases of HDS-associated liver injury are due to multi-ingredient nutritional sup

135 on to liver regeneration and repair in acute liver injury are lacking so far.

136 cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive immune system

137 eight by this slow process in the absence of liver injury are not as well understood.

138 and magnitude of these changes to the ECM in liver injury are poorly understood.

139 dup GBH formulation showed signs of enhanced liver injury as indicated by anatomorphological, blood/u

140 second more chronic model of alcohol-induced liver injury, as demonstrated by decreased serum alanine

141 ator of necroptosis, exacerbated HFD-induced liver injury, associated with increased inflammation and

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

143 However, direct APAP hepatoxicity and liver injury at early times post-APAP overdose were unaf

144 uld help stratify patients for their risk of liver injury at hospital presentation.

145 ipopolysaccharide/GalN-induced apoptosis and liver injury at the early time point, but this protectio

146 l of miR-122, HMGB1, and K18 predicted acute liver injury better than ALT alone (cfNRI 1.95 [95% CI 1

147 ntly down-regulated in three mouse models of liver injury (bile duct ligation, 1% cholic acid [CA] fe

148 etween modeled historical PFOA exposures and liver injury biomarkers and medically validated liver di

149 ogic studies suggest PFOA is associated with liver injury biomarkers.

150 rial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepa

151 n is a spontaneous process that occurs after liver injury, but acute liver failure is a complex and f

152 ays an important cytoprotective role against liver injury, but its mechanism is not fully determined.

153 tation into mice with genetically engineered liver injury, but these systems involve a long and varia

154 Acute liver injury can be secondary to a variety of causes, in

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

156 In response to liver injury, colony-stimulating factor 1 drives early m

157 KO mice were protected against APAP-induced liver injury compared with wild type mice.

158 1 (HMGB1), is a key regulator of a range of liver injury conditions and is elevated in clinical and

159 Sera from mice with acetaminophen-induced liver injury contained high levels of soluble B7 compare

160 Liver injury correlated positively with the degree of he

161 F19 and M70 rapidly and effectively reversed liver injury, decreased hepatic inflammation, attenuated

162 hat lipopolysaccharide/galactosamine-induced liver injury depends on hepatocyte-intrinsic TNF recepto

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

164 minate ALF (23%), idiosyncratic drug-induced liver injury DILI (22%), acute hepatitis B virus infecti

165 Liver biology and function, drug-induced liver injury (DILI) and liver diseases are difficult to

166 The association of drug-induced liver injury (DILI) and Stevens-Johnson syndrome (SJS) o

167 investigated the role of JNK in drug-induced liver injury (DILI) in liver tissue from patients and in

168 Drug-induced liver injury (DILI) is a major public health concern, an

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

170 Drug-induced liver injury (DILI) presents a significant challenge to

171 Drug-induced liver injury (DILI) remains a leading cause of drug with

172 r diseases are mainly caused by drug-induced liver injury (DILI).

173 with positive rechallenge after drug-induced liver injury (DILI): antimicrobials; and central nervous

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

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

176 lysaccharide (LPS) model of acute, fulminant liver injury dramatically decreased serum alanine aminot

177 MC-2 was associated with decreased liver injury, enhanced effective hepatic blood flow, dec

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

179 The 300 mg/kg Geniposide caused liver injury evidenced by pathological changes and incre

180 Hepatic stellate cell (HSC) activation on liver injury facilitates fibrosis.

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

182 kedly inhibited sustained JNK activation and liver injury from acetaminophen or tumor necrosis factor

183 ed hepatic macrophages and partially blocked liver injury from GalN/TNF.

184 -, herbal-, or dietary-supplement-associated liver injury had bile duct loss on liver biopsy, which w

185 As the role of this NOX in early alcoholic liver injury has not been addressed, we studied NOX4-med

186 Liver injury, hepatic lipid accumulation, and proinflamm

187 In severe liver injury, hepatocyte proliferation is impaired-a fea

188 In ischemic liver injury, hepatocyte-derived Gal-9 is both diagnosti

189 matory cells is a major feature of alcoholic liver injury however; the signals and cellular sources r

190 gnaling drives intrahepatic inflammation and liver injury in Con A hepatitis.

191 estore ConA-mediated NKT cell activation and liver injury in GF mice.

192 affect the incidence of alphaGalCer-induced liver injury in GF mice.

193 r injury in mice is a model for drug-induced liver injury in humans.

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

195 RT1720 administration alleviates cholestatic liver injury in mice by increasing hydrophilicity of hep

196 Acetaminophen-induced liver injury in mice is a model for drug-induced liver i

197 of Kupffer cells, as well as ethanol-induced liver injury in mice.

198 has recently been shown to potently prevent liver injury in murine models of ALD.

199 nvestigator assessment) were reported in two liver injury in one patient (<1%) in the olaparib plus p

200 enzyme, a key biomarker for the detection of liver injury in patients (with HIV and tuberculosis) who

201 pregulation of CYP3A4 may promote BA-induced liver injury in PSC.

202 (53%) were considered convincingly linked to liver injury in published case reports; 48 (13%) were as

203 tion of apoptosis partially protects against liver injury in response to a high-fat diet (HFD).

204 suggesting that liver fat is responsible for liver injury in the absence of other disease processes.

205 or generating new hepatocyte lineages during liver injury in the context of hepatotoxin-inhibited hep

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

207 t for severe alcoholic hepatitis must target liver injury in the short term and alcohol consumption i

208 United States and worldwide, and HDS-induced liver injury in the United States has increased proporti

209 n was still remarkably effective in blocking liver injury in this model.

210 (HS) chains, but the importance of HSPGs in liver injury in vivo remains unknown.

211 in culture and in a mouse model of alcoholic liver injury in vivo, and its expression correlates with

212 nd type I IFN-independent pathway of sterile liver injury in which hepatocytes are both the targets o

213 CCl4)-induced fibrosis and LPS-induced acute liver injury in wild-type (WT) and B6.B10ScN-Tlr4(lps-de

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

215 blood EVs from three other models of chronic liver injury, including bile duct ligation, nonalcoholic

216 Markers of liver injury, including serum alanine transaminase level

217 c platelet accumulation promote APAP-induced liver injury, independent of platelet PAR-4 signaling.

218 The primary endpoint was acute liver injury indicating need for continued acetylcystein

219 rces of CTGF and integrin alphavbeta6 during liver injury induced by 3,5-diethoxycarbonyl-1,4-dihydro

220 erein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcohol feedi

221 ic ablation of TPL2 in the mouse ameliorates liver injury induced by Con A and impinges on hallmarks

222 patoprotective potential against cholestatic liver injury induced by hepatotoxin such as ANIT.

223 d that PTX3 treatment attenuated LPS-induced liver injury, inflammation, and cell recruitment.

224 this reduction was associated with decreased liver injury, inflammation, and fibrosis.

225 Drug-induced liver injury is an important clinical entity resulting i

226 Drug rechallenge following drug-induced liver injury is associated with up to 13% mortality in p

227 Acute-on-chronic liver injury is characterized by an important inflammato

228 An identified cause for liver injury is lacking in approximately 30% of cases.

229 Amplification of liver injury is mediated by macrophages but the signalin

230 HBV infection is noncytopathic, and liver injury is mostly contributed by host immune respon

231 y which the macrophage inflammasome enhances liver injury is not completely understood.

232 endent pathway of cell death, to HFD-induced liver injury is not known.

233 The liver injury is propagated by lipotoxicity and is associ

234 duct loss during the course of drug-induced liver injury is uncommon, but can be an indication of va

235 significance of endogenous IL-22BP in acute liver injury is unknown.

236 ement in assessing causality in drug-induced liver injury is whether the implicated agent is known to

237 ide (LPS) is implicated in acute and chronic liver injury; its effects are mediated predominantly via

238 Liver injury leads to a vasculopathy in which post-trans

239 This transcriptional response to cholestatic liver injury likely promotes partial de-differentiation

240 - or MCD diet-induced liver inflammation and liver injury, likely as a result of increased production

241 Although liver injury markers and triglyceride content were simil

242 Liver injury markers were measured in serum, triglycerid

243 the complexity of idiosyncratic drug-induced liver injury means that no current single-cell model, wh

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

245 ndrial function in isolated mitochondria and liver injury models in vivo.

246 Using sterile liver injury models, we show that the STAT3-IL-10-IL-6 a

247 Liver injury modulates local microenvironment, triggerin

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

249 HDS-induced liver injury now accounts for 20% of cases of hepatotoxi

250 Liver fibrosis results from chronic liver injury of different etiologies.

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

252 elected patients with otherwise fatal severe liver injuries, particularly in whom cross-clamping with

253 The exuberant liver injury phenotypes in syndecan-1 null (Sdc1(-/-) )

254 ced infiltration of monocytes and attenuated liver injury post-APAP overdose at early time points.

255 HDS-induced liver injury presents many clinical and research challen

256 by rapamycin protects from EtOH-LPS-induced liver injury, probably through reduced macrophage expres

257 mmune responses to virus infection and acute liver injury, providing a new paradigm for viral pathoge

258 Infusions of HSCs into mice with liver injury reduced liver scarring based on picrosirius

259 After liver injury, regeneration occurs through self-replicati

260 tive liver damage, secondary to any cause of liver injury, results in progressive fibrosis, disrupted

261 n of those patients who develop severe acute liver injury (sALI) or acute liver failure (ALF) remain

262 y response in cholestasis and other forms of liver injury should lead to discovery of new therapeutic

263 mind, drug-targeting mechanisms involved in liver injury should only be tested for the short-term pe

264 (Deltahepa) mice produced a greater level of liver injury than that observed in Jnk1(Deltahepa) or co

265 ther cancers, hepatic Akt inhibition induces liver injury that could promote HCC.

266 ged cholestatic but ultimately self-limiting liver injury that has a distinctive serum biochemical as

267 PHB1 is an important mediator of cholestatic liver injury that regulates the activity of HDAC4, which

268 liver inflammatory responses and ameliorated liver injury that would normally occur following the eth

269 f FcRn results in resistance to APAP-induced liver injury through increased albumin loss into the bil

270 luated in a mouse model of LPS-induced acute liver injury to determine its S1P1-binding specificity.

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

272 sera of patients with ALF and from mice with liver injury to have high concentrations of soluble B7,

273 ation products play a role in progression of liver injury to steatohepatitis in NASH produced by high

274 , loss of beta1-integrin in hepatocytes with liver injury triggered a ductular reaction of cholangioc

275 represents a therapeutic target in steatotic liver injury, underlining the importance of development

276 an-1 in mice led to unopposed progression of liver injury upon APAP overdose.

277 epatoprotection and gave rise to exacerbated liver injury upon insult.

278 re resistant to the development of fulminant liver injury upon lipopolysaccharide administration.

279 ontrols, and mice with acetaminophen-induced liver injury using enzyme-linked immunosorbent assays.

280 r antigen were evaluated by Western Blot and liver injury was assessed by ALT and histology.

281 Acute liver injury was assessed in the murine Con A hepatitis

282 HAV-induced liver injury was associated with interferon-independent

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

284 Liver injury was measured 6 hours after reperfusion.

285 fed MCD sucrose-oleate, yet their degree of liver injury was much lower.

286 the derivation and validation cohorts, acute liver injury was predicted at hospital presentation by m

287 e of Gal3 in the pathogenesis of cholestatic liver injury, we generated dnTGF-betaRII/galectin-3(-/-)

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

289 the diagnosis and management of HDS-induced liver injury were the focus of a 2-day research symposiu

290 r, murine models of fibrotic and cholestatic liver injury were used to demonstrate that this approach

291 closely integrated during TNF-alpha-induced liver injury when both caspases and NF-kappaB are blocke

292 nged the mean survival time and resolved the liver injury when compared to the no-transplantation con

293 CES1 axis that regulates cholesterol-induced liver injury, which provides novel insights that improve

294 neration in the murine model of APAP induced liver injury, which was associated with a metabolic swit

295 rbated alcohol-induced hepatic steatosis and liver injury, which was associated with increased activa

296 conclusion, 300 mg/kg Geniposide can induce liver injury with associated changes in bile acid regula

297 is characterized by the progressive onset of liver injury with ductular reaction and fibrosis.

298 tures, and outcomes of cases of drug-induced liver injury with histologically proven bile duct loss.

299 Liver injury with portal hypertension was established us

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