ライフサイエンスコーパス: liver fibrosis

1 be developed for treatment of patients with liver fibrosis.

2 o hepatic stellate cell (HSC) activation and liver fibrosis.

3 of cell populations to the myofibroblasts in liver fibrosis.

4 ta, pulmonary fibrosis, aplastic anemia, and liver fibrosis.

5 therapeutic approaches to the management of liver fibrosis.

6 g-term treatment of chronic diseases such as liver fibrosis.

7 fibrosis in rat BDL and mouse CCl4 models of liver fibrosis.

8 with ballooning hepatocytes and significant liver fibrosis.

9 idin inhibits HSC activation and ameliorates liver fibrosis.

10 ated M2 macrophage activation and associated liver fibrosis.

11 re performed and compared for the staging of liver fibrosis.

12 for clinical translation into a therapy for liver fibrosis.

13 oblasts in fibrotic mouse livers and reduced liver fibrosis.

14 the role of KCa3.1 in experimental and human liver fibrosis.

15 juries and functions to restrict and resolve liver fibrosis.

16 ecific ferroportin deletion also ameliorates liver fibrosis.

17 R-200a is associated with the development of liver fibrosis.

18 tension and dyslipidemia and may progress to liver fibrosis.

19 ng miR-378a-3p has therapeutic potential for liver fibrosis.

20 hioacetamide treatment induced two phases of liver fibrosis.

21 atocyte death, inflammation, and progressive liver fibrosis.

22 sible for the decrease in FSAP expression in liver fibrosis.

23 ctive in transducing MFs in a mouse model of liver fibrosis.

24 ibition of either pathway in vivo attenuates liver fibrosis.

25 tential and attractive therapeutic target in liver fibrosis.

26 d iNOS induction, bile duct hyperplasia, and liver fibrosis.

27 inflammation in hepatitis C, and thereby for liver fibrosis.

28 ting, communicating diagnoses, and assessing liver fibrosis.

29 and ASFs from fibrotic tissue to ameliorate liver fibrosis.

30 onic HCV-associated immune dysregulation and liver fibrosis.

31 (serum HCV RNA >/=2000 IU/mL), and stage 3-4 liver fibrosis.

32 , a gene linked to bile duct hyperplasia and liver fibrosis.

33 lent rates of cure in patients with advanced liver fibrosis.

34 o be broadly efficacious in the treatment of liver fibrosis.

35 feration of primary hepatocytes, and reduces liver fibrosis.

36 t associated with progression to significant liver fibrosis.

37 es hepatocellular function, and might reduce liver fibrosis.

38 the deleterious actions of PAR2 in promoting liver fibrosis.

39 ew tractable therapeutic target for treating liver fibrosis.

40 ps with advanced alcoholic liver disease and liver fibrosis.

41 is angiogenic response and the resolution of liver fibrosis.

42 investigated the involvement of S1P in human liver fibrosis.

43 fusion-weighted MR imaging in the staging of liver fibrosis.

44 aluated within the noninvasive prediction of liver fibrosis.

45 Angiogenesis is a key feature of liver fibrosis.

46 stance, and TE values indicative of advanced liver fibrosis.

47 nificant therapeutic benefit in ameliorating liver fibrosis.

48 id degradation, and their deficiency induces liver fibrosis.

49 stage disease as well as those with advanced liver fibrosis.

50 of previous treatment status and underlying liver fibrosis.

51 maintaining liver homeostasis and preventing liver fibrosis.

52 ation and contributes to the pathogenesis of liver fibrosis.

53 timate the association of alcohol abuse with liver fibrosis.

54 ommendations on design of clinical trials in liver fibrosis.

55 Autophagy is a regulatory pathway in liver fibrosis.

56 inhibition protected mice from CCl4-induced liver fibrosis.

57 hepatic knockdown of GnRH decreased IBDM and liver fibrosis.

58 recommendations on clinical trial design for liver fibrosis.

59 ach to the noninvasive assessment of diffuse liver fibrosis.

60 ccuracy of the imaging parameters in staging liver fibrosis.

61 ivated HSCs might be a mechanism of limiting liver fibrosis.

62 stellate cells to promote the resolution of liver fibrosis.

63 after CM-101 injection was used to quantify liver fibrosis.

64 d alpha-SMA expression in an animal model of liver fibrosis.

65 ndMT in tissues from patients with end-stage liver fibrosis.

66 onalcoholic steatohepatitis and stage 2 or 3 liver fibrosis.

67 Cs) is a critical step in the development of liver fibrosis.

68 ways is critical to the roles of TGF-beta in liver fibrosis.

69 s, and finally in a significant reduction of liver fibrosis.

70 involve in the hepatoprotection conferred by liver fibrosis.

71 ling pathway could be a potential target for liver fibrosis.

72 f liver cancer is its close association with liver fibrosis.

73 l dystrophy, fibrocystic kidney disease, and liver fibrosis.

74 SE MR elastographic sequences for assessing liver fibrosis.

75 etes, reported higher prevalence of advanced liver fibrosis (0-27.9%) and cirrhosis (2.4-4.0%) than t

76 More focused stratification for advanced liver fibrosis (0.9-2.0%) or cirrhosis (0.1-1.7%) narrow

77 Liver fibrosis, a form of scarring, develops in chronic

78 Mesenchymal stromal cells and liver fibrosis: a complicated relationship.

79 CoQ10 supplementation prevented liver fibrosis accompanied by downregulation of oxidativ

80 ies have indicated the favourable effects of liver fibrosis against acute insults.

81 The level of liver fibrosis also correlated between monozygotic twins

82 ricellular protein that dampens and resolves liver fibrosis, also mediates cholangiocyte proliferatio

83 The early detection of liver fibrosis among patients with nonalcoholic fatty li

84 However, liver fibrosis, an IL-13-mediated pathological consequen

85 our understanding of the pathophysiology of liver fibrosis and a large number of potential cellular

86 ce of the TLR4/LPS-independent mechanisms of liver fibrosis and also indicate that TLR4 is not entire

87 ion of biliary mass, along with reduction of liver fibrosis and angiogenesis.

88 ATX is a novel player in the pathogenesis of liver fibrosis and cancer and a promising therapeutic ta

89 mitigating the HCV-related complications of liver fibrosis and cancer are yet largely unknown.

90 Using data from the PROLIFICA (Prevention of Liver Fibrosis and Cancer in Africa) program, we conduct

91 s known about its role and mode of action in liver fibrosis and cancer.

92 rlying HCV chronicity and the development of liver fibrosis and cancer.

93 g seroconversion, and prevent development of liver fibrosis and cancer.

94 If left untreated, cholestasis leads to liver fibrosis and cirrhosis, which eventually results i

95 ive and is associated with reduced levels of liver fibrosis and cirrhosis.

96 ve IFNL4 protein variant are associated with liver fibrosis and damage in a large multicenter cohort

97 raphy to be an excellent tool for diagnosing liver fibrosis and for excluding (ruling out rather than

98 stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC).

99 close to the hepatic scar in mouse models of liver fibrosis and in human liver disease.

100 tiviral therapy and decreased progression of liver fibrosis and incidence of HCC among a large cohort

101 CHF and 2) the association between stage of liver fibrosis and incident CHF is modified by HIV/HCV s

102 ER stress, couples hepatocyte apoptosis with liver fibrosis and indicate that innate immune signaling

103 ells, resulting in significantly ameliorated liver fibrosis and inflammation.

104 Genetic markers of liver fibrosis and inflammatory cytokines were significa

105 ns of low-dose NTBC, FAH(-/-) pigs developed liver fibrosis and portal hypertension, and thus may ser

106 Various parameters of liver fibrosis and potential mechanisms such as oxidativ

107 acologic targeting of LOX pathway to inhibit liver fibrosis and promote its resolution.

108 found that MSDC-0602 prevented and reversed liver fibrosis and suppressed expression of markers of s

109 n of the TGF-beta pathway is associated with liver fibrosis and suppression of liver tumorigenesis, c

110 expression was increased in rodent and human liver fibrosis and was predominantly observed in the hep

111 iciently depicts the presence of significant liver fibrosis and, less accurately, mild liver fibrosis

112 r or control before evaluating biliary mass, liver fibrosis, and angiogenesis.

113 in Mdr2(-/-) ablates biliary proliferation, liver fibrosis, and angiogenesis.

114 Further, ANIT-induced iNOS expression, liver fibrosis, and bile duct hyperplasia were significa

115 Cholestatic injury precedes liver fibrosis, and cholangiocytes interact with HSCs pr

116 destruction of the biliary system leading to liver fibrosis, and deterioration of liver function.

117 sma transaminase concentrations, ameliorated liver fibrosis, and improved hepatic protein synthetic f

118 between cell dysfunction, parainflammation, liver fibrosis, and macrophage polarization over time.

119 lcohol use was independently associated with liver fibrosis, and may better predict fibrosis progress

120 d tumor growth, reduced tumor malignancy and liver fibrosis, and prevented tumor development.

121 ntribute to myofibroblasts in peritoneal and liver fibrosis, and protection of the MC layer leads to

122 llent therapeutic agent for the treatment of liver fibrosis, and that FZHY treatment can enhance our

123 Melatonin levels, biliary mass, liver fibrosis, angiogenesis and miR-200b expression wer

124 Pathways of liver fibrosis are controlled by connective tissue growt

125 ase, with the use of non-invasive markers of liver fibrosis, are needed in the general population set

126 ations in serum SL levels and progression of liver fibrosis as well as responsiveness to antiviral th

127 ntact Nlrp3(A350V) mutants showed changes in liver fibrosis, as evidenced by morphometric quantitatio

128 account in order to avoid overestimations of liver fibrosis assessed by transient elastography.

129 r biopsy, noninvasive imaging modalities for liver fibrosis assessment have gained popularity.

130 atabase for Hepatitis B and C with CHC and a liver fibrosis assessment were eligible for inclusion.

131 to acquire liver stiffness measurements for liver fibrosis assessment.

132 According to the degree of liver fibrosis at liver biopsy, 88.5%-96.8% of patients

133 No strategies for detection of liver fibrosis at these early stages have been developed

134 (HSCs) are key players in the development of liver fibrosis, but the role of PNPLA3 and its variant I

135 of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately 50%.

136 med to study the role of CYP2E1 in promoting liver fibrosis by high cholesterol-containing fast-food

137 In summary, hepcidin suppresses liver fibrosis by impeding TGFbeta1-induced Smad3 phosph

138 IL-22 ameliorates liver fibrosis by inhibiting hepatic stellate cells (HSC

139 We aimed to determine whether prediction of liver fibrosis by LSM in NAFLD patients is affected by C

140 d are transient elastography-which estimates liver fibrosis by measuring liver stiffness-and serum bi

141 at CYP2E1 is important in fast food-mediated liver fibrosis by promoting nitroxidative and ER stress,

142 Patients underwent assessment of liver fibrosis by transient elastography (TE) and testin

143 Liver fibrosis can regress in patients with chronic hepa

144 The chronic hepatic inflammation leads to liver fibrosis, cirrhosis, and cancer in a significant n

145 dependent risk factor for the development of liver fibrosis/cirrhosis and hepatocellular carcinoma (H

146 Moderate and advanced liver fibrosis/cirrhosis are associated with an increase

147 PZ-235 significantly suppressed liver fibrosis, collagen deposition, inflammatory cytoki

148 Validated non-invasive tests for liver fibrosis consistently detected otherwise unrecogni

149 estimate of insulin resistance (HOMA-IR) and liver fibrosis defined using the aspartate aminotransfer

150 a, membranoproliferative glomerulonephritis, liver fibrosis, deforming arthropathy and increased anti

151 ase, and there is evidence that experimental liver fibrosis depends on bacterial translocation.

152 /-) mice were protected from malaria-induced liver fibrosis despite having a similar liver parasite b

153 Changes in noninvasive measures of liver fibrosis did not differ significantly between eith

154 prospective study of individuals at risk for liver fibrosis due to alcohol consumption, we found elas

155 Inhibition of KCa3.1 aggravated liver fibrosis during carbon tetrachloride challenge but

156 cells (HSCs) participate in the promotion of liver fibrosis during cholestasis.

157 M2 macrophage activation was associated with liver fibrosis during chronic HCV infection in the liver

158 ing macrophages/Kupffer cells, which mediate liver fibrosis during rodent malaria infections.

159 ) coinfection is associated with an enhanced liver fibrosis (ELF) score higher than that for uninfect

160 uated the prognostic utility of the enhanced liver fibrosis (ELF) score in Norwegian PSC patients.

161 Changes in Enhanced Liver Fibrosis (ELF) scores and serum bile acids were al

162 SSWE allows accurate assessment of liver fibrosis, even in children with early stage (F1-F2

163 efined as the change in Fibrosis-4 Index for Liver Fibrosis (FIB-4) units per year using random-inter

164 at link inflammation with the development of liver fibrosis, focusing on the role of inflammatory med

165 e also given injections of CCl4, to increase liver fibrosis, for 8 weeks.

166 ver specimens from patients with cholestatic liver fibrosis had increased numbers of MSLN+ aPFs/myofi

167 HCV-infected women with stage 3-4 liver fibrosis had lower mean z scores for trabecular vo

168 use of cost, treatment is often denied until liver fibrosis has progressed to at least moderate fibro

169 Non-invasive methods for assessing liver fibrosis have been developed, of which the most co

170 ucing receptors; their differential roles in liver fibrosis have not been investigated.

171 cell count, antiretroviral therapy, HIV RNA, liver fibrosis, HCV genotype, and exposure to specific a

172 the Mdr2 -/- mouse model of advanced biliary liver fibrosis how the subcutaneously injected microsphe

173 est in the use of bone marrow cells to treat liver fibrosis, however, little is known about their ant

174 cts on cell behavior and is increased during liver fibrosis; however, its effect on primary hepatocyt

175 us (HCV) coinfection accelerates progressive liver fibrosis; however, the mechanisms remain poorly un

176 y, CcnE1-siRNA also prevented progression of liver fibrosis if applied after onset of chronic liver i

177 t elastography accuracy for the diagnosis of liver fibrosis in a cohort of consecutive patients with

178 and may induce a biopsy-proven regression of liver fibrosis in a liver transplant recipient with cirr

179 GH resistance dramatically exacerbates liver fibrosis in a mouse model of inflammatory cholesta

180 Prolonged darkness reduces liver fibrosis in a mouse model of primary sclerosing ch

181 , and to assess its ability to help quantify liver fibrosis in animal models.

182 ete darkness reduces biliary hyperplasia and liver fibrosis in bile-duct-ligated (BDL) rats; however,

183 tant in the management of biliary damage and liver fibrosis in cholangiopathies including PSC.

184 hether treatment can achieve a regression of liver fibrosis in chronic HEV patients.

185 The purpose of our study was to investigate liver fibrosis in conventional and germ-free (GF) C57BL/

186 r communication in the activation of HSC for liver fibrosis in HCV infection.IMPORTANCE HCV-associate

187 between IFN-lambda genotypes and significant liver fibrosis in HIV-HCV coinfection.

188 tic activity and is associated with enhanced liver fibrosis in humans.

189 estly (approximately two- to five-fold) with liver fibrosis in mice and humans, demonstrating specifi

190 ial-to-mesenchymal transition and consequent liver fibrosis in mice via a SMAD3-dependent mechanism.

191 tor VII-activating protease (FSAP) increases liver fibrosis in mice.

192 sponse of hematopoietic stem cells (HSCs) to liver fibrosis in mice.

193 SSI provide high value for the diagnosis of liver fibrosis in NAFLD patients.

194 SM) frequently overestimates the severity of liver fibrosis in nonalcoholic fatty liver disease (NAFL

195 relevant hypotheses for the pathogenesis of liver fibrosis in patients with HIV/HCV coinfection that

196 findings suggest that selonsertib may reduce liver fibrosis in patients with nonalcoholic steatohepat

197 nt liver fibrosis and, less accurately, mild liver fibrosis in pediatric patients with nonalcoholic f

198 ce that human genetic variants contribute to liver fibrosis in subjects with hepatitis C virus (HCV)

199 ata suggest that programmes of screening for liver fibrosis in the general population should be asses

200 prevalence of, and factors associated with, liver fibrosis in the general population, we aimed to in

201 otic livers, suggesting an important role of liver fibrosis in the premalignant environment (PME) of

202 lay between IL-22 and miR-200a in regulating liver fibrosis in vivo and in vitro.

203 Importantly, FAK inhibitor attenuates liver fibrosis in vivo and significantly reduces collage

204 alpha-naphthylisothiocyanate (ANIT)-induced liver fibrosis increased in Fibgamma(390-396A) mice, whe

205 play a critical role in the pathogenesis of liver fibrosis induced by bile duct ligation (BDL).

206 Liver fibrosis induced by carbon tetrachloride is attenu

207 iral delivery of hepcidin to mice attenuates liver fibrosis induced by CCl4 treatment or bile duct li

208 Purpose To determine the relationship of liver fibrosis, inflammation, and steatosis with the mag

209 formed to determine the relationship between liver fibrosis, inflammation, steatosis, and alanine ami

210 s in HCV infection.IMPORTANCE HCV-associated liver fibrosis is a critical step for end-stage liver di

211 Acute injury in the setting of liver fibrosis is an interesting and still unsettled iss

212 Liver fibrosis is associated with a decrease in FSAP exp

213 Cholestatic liver fibrosis is caused by obstruction of the biliary t

214 Liver fibrosis is characterized by the persistent deposi

215 Liver fibrosis is common, particularly in individuals wh

216 nding the underlying molecular mechanisms of liver fibrosis is important to develop effective therapy

217 bjectives were to assess whether 1) stage of liver fibrosis is independently associated with incident

218 iagnosis is rarely made in early stages-when liver fibrosis is mild to moderate but cirrhosis is not

219 Liver fibrosis is the most important predictor of mortal

220 s cellular processes; however, their role in liver fibrosis is unclear.

221 However, prior studies of estrogen and liver fibrosis lack serial fibrosis measures, adjustment

222 Progressive liver fibrosis leads to portal hypertension and liver fa

223 he relationship between blood microbiota and liver fibrosis (LF) in European cohorts of patients with

224 errant in many pathologies, its relevance in liver fibrosis (LF) remained unexplored.

225 ), a direct antifactor Xa, on HSC phenotype, liver fibrosis (LF), liver microthrombosis, and PH in ci

226 Our findings demonstrated that liver fibrosis manifested a beneficial role for host sur

227 ecreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in serum and tissues, and improve

228 DM and obesity, this study illustrates that liver fibrosis may become a more prominent public health

229 Non-invasive tests of liver fibrosis might provide a mechanism for earlier dia

230 ntrol hepatotropic pathogens and suggest how liver fibrosis might reduce CD8 TE immune surveillance t

231 intermittently elevated transaminase levels, liver fibrosis, mild ataxia, and cognitive impairment.

232 In a murine liver fibrosis model enhanced carrier and payload accumu

233 Our liver fibrosis model estimated that the increase in slau

234 natures were significantly induced in rodent liver fibrosis models (n = 3-5) and in human samples of

235 population without known liver disease have liver fibrosis, mostly associated with non-alcoholic fat

236 Liver fibrosis occurs through a mechanism of HSC-mediate

237 sistent HCV infection and advanced stages of liver fibrosis or cirrhosis and 20 controls with fatty l

238 detection among HBsAg-positive patients with liver fibrosis or hepatocellular carcinoma was 5.24 (95%

239 EphB family of receptor tyrosine kinases in liver fibrosis or in the pathogenesis of malaria infecti

240 ults SWE showed a very high correlation with liver fibrosis (P < .001) at univariate and multivariate

241 hepatic CoQ10 concentrations and ameliorated liver fibrosis (P < 0.001), inflammation (P < 0.001), so

242 n between neutralization breadth and reduced liver fibrosis (P= 0.006).

243 y 2 to 3 months postinfection, hepatitis and liver fibrosis persisted after clearance.

244 Liver fibrosis, portal pressure, and hepatic tumor burde

245 cl-xL-specific inhibitor, A-1331852, reduces liver fibrosis, possibly by a dual effect on activated f

246 Liver fibrosis progresses faster in individuals coinfect

247 he aim of this study was to compare rates of liver fibrosis progression (measured by the aspartate-to

248 p between sustained virological response and liver fibrosis progression among persons infected with h

249 contributes to collagen stabilization during liver fibrosis progression and limits spontaneous fibros

250 d the first genome-wide association study of liver fibrosis progression in patients coinfected with H

251 nabinol [THC]") use has been associated with liver fibrosis progression in retrospective analyses of

252 tellate cells (HSCs) activation in vitro and liver fibrosis progression in vivo.

253 Our main outcomes were liver fibrosis progression measured by FIB-4 scores, SVR

254 Liver fibrosis progression was more influenced by the ba

255 lays an essential role in HSC activation and liver fibrosis progression, and FAK signaling pathway co

256 e may not be required to prevent accelerated liver fibrosis progression.

257 s significantly to collagen stabilization in liver fibrosis, promotes fibrogenic activation of attenu

258 Significant liver fibrosis remains an impediment to achieving SVR wi

259 Natural killer (NK) cells can induce liver fibrosis remission by killing hepatic stellate cel

260 Initiation and progression of liver fibrosis requires proliferation and activation of

261 Liver fibrosis results from chronic liver injury of diff

262 In the United States population, higher liver fibrosis scores were associated with increased liv

263 We examined whether liver fibrosis scores were associated with increased ove

264 est that the ELF score can be used to assess liver fibrosis severity in HIV-infected women.

265 study identified a new locus associated with liver fibrosis severity in patients with HIV/HCV coinfec

266 By multivariate analysis, liver fibrosis stage 0-1 (OR = 5.00; 95% CI, 2.02-12.37;

267 It remains unknown whether liver fibrosis stage influences the CHF risk or if HIV o

268 e more accurate than TE in identification of liver fibrosis (stage 1 or more), using biopsy analysis

269 ter receiving elafibranor 120 mg had reduced liver fibrosis stages compared with those without NASH r

270 sition in mice with progressive and advanced liver fibrosis that received cationic lipid nanoparticle

271 In rats with advanced liver fibrosis, the Emax, Tmax, HEF, and MRT decreased s

272 rome characterized by lung, bone marrow, and liver fibrosis; these findings extend the phenotype of P

273 L-22 inhibits HSC activation and ameliorates liver fibrosis through enhancing expression of miR-200a

274 stages of HCV+ hepatic lesions, from minimal liver fibrosis to cirrhosis and HCC, compared to histolo

275 on of fibrotic septa, and the progression of liver fibrosis to cirrhosis.

276 r established HBV-persistent mouse line with liver fibrosis to evaluate the efficacy of novel therapi

277 Here, we use experimental models of liver fibrosis to show that deficiency of the scavenger

278 EphB2 expression promotes malaria-associated liver fibrosis; to our knowledge, our data are the first

279 ovides a novel target for the development of liver fibrosis treatments.

280 r, SOT was not associated with a progressive liver fibrosis up to 5 years.

281 e apoptosis and liver injury, accompanied by liver fibrosis upon repeated administration of CCl4 Defi

282 The prevalence of liver fibrosis varied between 0.7% and 25.7%.

283 ASH phenotype, both independently benefitted liver fibrosis via altered hepatic stellate cell activat

284 nnate immune signaling regulates outcomes of liver fibrosis via modulation of hepatocyte death in the

285 Liver fibrosis was assessed by elastography (FibroScan),

286 Liver fibrosis was assessed by means of liver biopsy, tr

287 Liver fibrosis was assessed histologically by liver biop

288 Inhibition of let-7a accelerated liver fibrosis was attributed to cholestasis.

289 Liver fibrosis was categorized according to FIB-4 scores

290 the proton-density fat fraction (MRI-PDFF); liver fibrosis was measured based on stiffness measured

291 Liver fibrosis was measured using the fibrosis 4 index (

292 Liver fibrosis was predicted using the aspartate aminotr

293 A gradual regression of liver fibrosis was reported (Metavir A0/F1 in 2015 versu

294 n our efforts to generate a new medicine for liver fibrosis, we sought to identify improved small mol

295 d role of macrophages in chronic HCV-induced liver fibrosis, we utilized a recently developed humaniz

296 varying levels of diethylnitrosamine-induced liver fibrosis were imaged before and 45 minutes after i

297 participants with HCV (GT-1) and early-stage liver fibrosis who previously failed 4-6 weeks of LDV/SO

298 Hepatocyte death is required for liver fibrosis with causal involvement of STING and IRF3

299 A trend toward decreased liver fibrosis with endothelial cell therapy was observe

300 For induction of liver fibrosis, WT mice were challenged with CCl4 for 4-