ライフサイエンスコーパス: liver fibrosis

1 as such are important in the progression of liver fibrosis.

2 , and a measure (L(f) ) was used to quantify liver fibrosis.

3 Loss of Ezh1 and Ezh2 also resulted in liver fibrosis.

4 f early ART in preventing the development of liver fibrosis.

5 al regulator to deactivate aHSCs and resolve liver fibrosis.

6 is and shares environmental correlation with liver fibrosis.

7 itis C virus treatment on the progression of liver fibrosis.

8 tion, hepatocellular injury, and progressive liver fibrosis.

9 n at S80 might be developed for treatment of liver fibrosis.

10 e progression of alcoholic liver disease and liver fibrosis.

11 ated in clinically relevant animal models of liver fibrosis.

12 nhibition of TNFR signaling protects against liver fibrosis.

13 d not reduce liver fat content or markers of liver fibrosis.

14 ule agonist of the relaxin receptor ML290 in liver fibrosis.

15 e Mdr2-/- mouse model of progressive biliary liver fibrosis.

16 holic steatohepatitis (NASH) and significant liver fibrosis.

17 on; FXR and TGR5 DKO mice may be a model for liver fibrosis.

18 m2 and activation of ADAM17 increased during liver fibrosis.

19 for a relationship between lung function and liver fibrosis.

20 oliferation or senescence, inflammation, and liver fibrosis.

21 lls (HSCs) contributes to the development of liver fibrosis.

22 2.67 defined patients with risk for advanced liver fibrosis.

23 strointestinal bleeding, kidney failure, and liver fibrosis.

24 d consequently biliary tree inflammation and liver fibrosis.

25 jections of CCl(4) to induce non-cholestatic liver fibrosis.

26 Hepatocarcinogenesis is tightly linked to liver fibrosis.

27 s protects mice from DDC-induced cholestatic liver fibrosis.

28 or developed for treatment of patients with liver fibrosis.

29 ll marker, to treat liver adenocarcinoma and liver fibrosis.

30 , ML290 demonstrated antifibrotic effects in liver fibrosis.

31 hosphorylation of MECP2 on HSC phenotype and liver fibrosis.

32 hepatic stellate cells, which may result in liver fibrosis.

33 ntitis may be an independent risk factor for liver fibrosis.

34 ccuracy of the imaging parameters in staging liver fibrosis.

35 stellate cells to promote the resolution of liver fibrosis.

36 involve in the hepatoprotection conferred by liver fibrosis.

37 be developed for treatment of patients with liver fibrosis.

38 atocyte death, inflammation, and progressive liver fibrosis.

39 tential and attractive therapeutic target in liver fibrosis.

40 and ASFs from fibrotic tissue to ameliorate liver fibrosis.

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

42 hepatic knockdown of GnRH decreased IBDM and liver fibrosis.

43 ed liver fibrosis, and 20 with mild-moderate liver fibrosis.

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

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

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

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

48 onalcoholic steatohepatitis and stage 2 or 3 liver fibrosis.

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

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

51 ore pronounced in persons with more advanced liver fibrosis.

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

53 s and enhances the inflammatory reaction and liver fibrosis.

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

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

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

57 SE MR elastographic sequences for assessing liver fibrosis.

58 is the reference test for the assessment of liver fibrosis.

59 er biochemistry and/or clinical suspicion of liver fibrosis.

60 or were given carbon tetrachloride to induce liver fibrosis.

61 sts and immune cells, followed by aggressive liver fibrosis.

62 hepatic stellate cells that are involved in liver fibrosis.

63 inflammation, renal injury/dysfunction, and liver fibrosis.

64 role for miR-31 (MIR31) in TGF-beta1-induced liver fibrosis.

65 ith advanced compared with earlier stages of liver fibrosis.

66 negative hepatitis D patients with advanced liver fibrosis.

67 SUMOylation inhibitors and FXR agonists for liver fibrosis.

68 of inflammation, hepatocyte ballooning, and liver fibrosis.

69 epatic bile duct obstruction and progressive liver fibrosis.

70 Liver elastography has been used to stage liver fibrosis.

71 s are used to identify persons with advanced liver fibrosis.

72 (HSCs) and in vivo models of CCl(4)-induced liver fibrosis.

73 significantly correlated with the degree of liver fibrosis.

74 deliver therapeutic agents to aHSC to treat 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 common outcome of chronic liver diseas

78 We observed increased liver fibrosis, accelerated disease progression, and an

79 Mice with liver fibrosis after BDL had increased hepatic PFKFB3; i

80 e of activated stellate cells and alleviated liver fibrosis after BDL.

81 Future studies should assess whether liver fibrosis among those with HIV viral suppression an

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

83 rgets cholangiocytes and is characterized by liver fibrosis and biliary proliferation.

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

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

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

87 knockout of SM alpha-actin leads to reduced liver fibrosis and COL1 expression.

88 DR is associated with liver fibrosis and damage, and the extent of DR parallel

89 Liver fibrosis and fibrosis-associated hepatocarcinogene

90 HIV-HCV-coinfected patients independently of liver fibrosis and HCV cure.

91 s of chronic hepatitis C virus (HCV)-induced liver fibrosis and hepatocarcinogenesis are still poorly

92 oral administration of SPD protects against liver fibrosis and hepatocarcinogenesis through activati

93 ively, our results confirm that OPN promotes liver fibrosis and highlight Fam20C as a novel factor dr

94 hese tools are already in use for evaluating liver fibrosis and in the assessment of focal lesions in

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

96 NAC also reduced bile duct obstruction and liver fibrosis and increased survival times.

97 oint to it being a key chemokine controlling liver fibrosis and inflammation in the context of YAP/TA

98 Early diagnosis and noninvasive detection of liver fibrosis and its heterogeneity remain as major unm

99 The growing burden of liver fibrosis and lack of effective antifibrotic therap

100 reatment was associated with lower levels of liver fibrosis and lower expression of fibrotic and infl

101 etection of early-stage (Ishak stage 3 of 6) liver fibrosis and nonalcoholic steatohepatitis (Ishak s

102 LCN2 contributes to liver fibrosis and portal hypertension in AH and could r

103 ) is an inhibitor of galectin 3 that reduces liver fibrosis and portal hypertension in rats and was s

104 ears suitable for the sustained treatment of liver fibrosis and possibly other chronic diseases.

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

106 re can increases early detection of advanced liver fibrosis and reduce unnecessary referral of patien

107 Liver fibrosis and renal dysfunction are common and may

108 Therapies to reduce liver fibrosis and stimulate organ regeneration are urge

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

110 The link between liver fibrosis and the natural history of COVID-19 shoul

111 atinib possessed therapeutic potency against liver fibrosis and the potential for application against

112 AI is also tested to assess liver fibrosis and to differentiate patients with pancre

113 s, DR can be a therapeutic target to inhibit liver fibrosis and to promote liver regeneration.

114 ekly doses of carbon tetrachloride to induce liver fibrosis and tumorigenesis.

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

116 onically infected with HCV, 39 with advanced liver fibrosis, and 20 with mild-moderate liver fibrosis

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

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

119 angiocytes, increases biliary proliferation, liver fibrosis, and bicarbonate secretion.

120 holic acid synthesis and the bile acid pool, liver fibrosis, and inflammation; FXR and TGR5 DKO mice

121 ts affected liver fat content, biomarkers of liver fibrosis, and the composition of the fecal microbi

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

123 e the association between lead poisoning and liver fibrosis as well as the change in the degree of li

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

125 association between PRO-C3 concentration and liver fibrosis assessed by magnetic resonance elastograp

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

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

128 ver disease to create a predictive model for liver fibrosis based upon a microbial signature.

129 At current drug prices, targeted testing and liver fibrosis-based treatment provided worse outcomes a

130 Decreased ductular reaction, liver fibrosis, biliary senescence, and biliary inflamma

131 ers of platelets were associated with higher liver fibrosis burden.

132 data suggest that FZHY ameliorates not only liver fibrosis but also vessel remodeling in experimenta

133 ol increased oxidative stress and markers of liver fibrosis but not hepatic steatosis in DKO mice.

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

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

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

137 or 3 mg, 25% and 42%, respectively, improved liver fibrosis by one stage or more without worsening of

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

139 f mice with bile duct ligation (BDL)-induced liver fibrosis, by monitoring echocardiography and intra

140 Liver fibrosis can regress in patients with chronic hepa

141 Lcn2(-/-) mice were protected from liver fibrosis caused by either ethanol or CCl(4) exposu

142 We found marked advance of liver fibrosis (chronic damage), as well as necrosis of

143 of chronic hepatitis, which often results in liver fibrosis, cirrhosis and hepatocellular carcinoma (

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

145 Those with advanced liver fibrosis/cirrhosis (N = 25) had higher HIV-1 RNA a

146 this study was to identify risk factors for liver fibrosis/cirrhosis in a cohort of Greek HIV-infect

147 We hypothesize that advanced liver fibrosis/cirrhosis is associated with alterations

148 Advanced liver fibrosis/cirrhosis was defined as FIB-4 > 3.25, AP

149 Advanced liver fibrosis/cirrhosis was not significantly associate

150 Advanced liver fibrosis/cirrhosis was not significantly associate

151 ts (LREs) were significantly correlated with liver fibrosis/cirrhosis.

152 er and represent an improved system to study liver fibrosis compared to two-dimensional mono- or co-c

153 d HSC activation and reduced the severity of liver fibrosis compared with mice given vehicle.

154 of an inflammatory infiltrate and pattern of liver fibrosis compatible with human NASH is desirable i

155 Liver fibrosis could not be diagnosed with ultrasound ex

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

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

158 bpopulation of macrophages, which expands in liver fibrosis, differentiates from circulating monocyte

159 cirrhotic liver tissues, rats and mice with liver fibrosis (due to bile duct ligation [BDL] or admin

160 axis in regulating biliary proliferation and liver fibrosis during cholestasis.

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

162 The enhanced liver fibrosis (ELF) index was validated against liver h

163 stimate the association between the Enhanced Liver Fibrosis (ELF) test and liver-related events (LRE)

164 FIB-4 for all patients followed by Enhanced Liver Fibrosis (ELF) test for patients with indeterminat

165 ography for test-positives, (2) the enhanced liver fibrosis (ELF) test with hospital liver stiffness

166 ST PRACTICE ADVICE 3: Patients with advanced liver fibrosis (F3) or cirrhosis at the time of DAA trea

167 ST PRACTICE ADVICE 2: Patients with advanced liver fibrosis (F3) or cirrhosis should receive surveill

168 had metabolic syndrome and 23% had advanced liver fibrosis (FIB-4 > 3.25).

169 ose inflammation, steatohepatitis (NASH) and liver fibrosis found in WT animals.

170 Most patients treated at an early stage of liver fibrosis had a stable low risk.

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

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

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

174 echanistic pathways that lead to accelerated liver fibrosis have not been well defined.

175 usions, secondary haemochromatosis, advanced liver fibrosis, heart failure, ACLF and death.

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

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

178 ibitor Y27632 to the key pathogenic cells in liver fibrosis, i.e. myofibroblasts including activated

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

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

181 effects of periodontal disease in promoting liver fibrosis in a rat model of ligature-induced period

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

183 axis triggers biliary damage/senescence and liver fibrosis in bile duct ligated and Mdr2(-/-) (alias

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

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

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

187 ceptor signaling mediates biliary damage and liver fibrosis in early-stage primary biliary cholangiti

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

189 ls whose activation triggers and perpetuates liver fibrosis in hepatocellular carcinomas.

190 CCR5 mutation and blockade on biomarkers of liver fibrosis in HIV-1 patients.

191 l population and markers of inflammation and liver fibrosis in Mdr2(-/-) and DKO mice.

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

193 ls (HSCs) and is required for development of liver fibrosis in mice.

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

195 titis (NASH) and contribute to toxin-induced liver fibrosis in mice.

196 (GalR2), in cholangiocyte proliferation and liver fibrosis in multidrug resistance protein 2 knockou

197 ype 3 procollagen (PRO-C3) is a biomarker of liver fibrosis in nonalcoholic fatty liver disease (NAFL

198 n shown to improve markers of metabolism and liver fibrosis in obese patients with type 2 diabetes.

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

200 entified factors associated with significant liver fibrosis in patients, which could facilitate hepat

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

202 therapy (ART) in reducing or contributing to liver fibrosis in persons with human immunodeficiency vi

203 strains of mice developed similar levels of liver fibrosis in response to CCl(4) exposure.

204 late cells, which reduces TNFR signaling and liver fibrosis in response to injury.

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

206 titis (NASH), alcohol-related cirrhosis, and liver fibrosis in those infected with viral hepatitis (B

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

208 an 5.3kPa (3.0-67.8), 25% having significant liver fibrosis including 12% with cirrhosis.

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

210 d SUMOylation inhibitors drastically impedes liver fibrosis induced by CCl(4), bile duct ligation, an

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

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

213 Liver fibrosis interferes with normal liver function and

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

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

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

217 Liver fibrosis is characterised by a dense and highly cr

218 Liver fibrosis is common, particularly in individuals wh

219 ivated hepatic stellate cell (aHSC)-mediated liver fibrosis is essential to the development of liver

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

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

222 restore tissue homeostasis in mice in which liver fibrosis is induced chemically or by diet.

223 In patients with NASH, liver fibrosis is the main determinant of mortality.

224 Liver fibrosis is the major determinant of liver related

225 Liver fibrosis is the most important predictor of mortal

226 or extracellular matrix protein important in liver fibrosis, is investigated with the results demonst

227 in mannose phosphate isomerase (MPI) develop liver fibrosis led us to explore the function of MPI and

228 rosis as well as the change in the degree of liver fibrosis, levels of inflammatory mediators and glu

229 RP3) inflammasome plays an important role in liver fibrosis (LF) development.

230 hereas 5HTR2B receptor antagonists attenuate liver fibrosis (LF) in mice.

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

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

233 ion in hepatic stellate cells (HSCs) reduces liver fibrosis (LF).

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

235 Alcohol-induced increases in early liver fibrosis markers (sirius red, hydroxyproline, and

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

237 Whether liver fibrosis might be a relevant player in the natural

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

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

240 Our liver fibrosis model estimated that the increase in slau

241 nfirmed using a carbon tetrachloride-induced liver fibrosis model in wild-type, Nrf2(-/-) , p62(-/-)

242 sis model, the mouse chronic schistosomiasis liver fibrosis model, as well as novel 2D and 3D human c

243 We applied the mouse CCl(4)-driven liver fibrosis model, the mouse chronic schistosomiasis

244 arcinomas, as well as in 2 independent mouse liver fibrosis models.

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

246 cal conditions such as rheumatoid arthritis, liver fibrosis, or obesity.

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

248 idence for the role of the microbiome in the liver fibrosis pathogenesis, especially in non-obese sub

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

250 an harvest one week later clearly attenuated liver fibrosis progression and significantly suppressed

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

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

253 for a benefit of early versus delayed ART on liver fibrosis progression.

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

255 VD deficiency is associated with liver fibrosis progression.

256 icity, serum PRO-C3 correlated strongly with liver fibrosis (r(2) = 0.50, P < 0.001) and demonstrated

257 disease, pulmonary endothelial dysfunction, liver fibrosis, renal disease, and exercise intolerance

258 Therefore, we hypothesize this endogenous liver fibrosis repair mechanism can be leveraged for liv

259 Using liver fibrosis resistant/susceptible mouse strain system

260 Liver fibrosis results from chronic liver injury of diff

261 ollagen (Pro-C3; -22% and -33%) and enhanced liver fibrosis score (ELF; -3% and -6%) at week 12.

262 , 1.00-1.02; P = 0.015), and higher enhanced liver fibrosis score (HR per unit, 1.26; 95% CI, 0.98-1.

263 .0 kPa in F3 disease, baseline mean Enhanced Liver Fibrosis score of 11.4 +/- 1.2 in F4 disease and 1

264 l of alpha-smooth muscle actin, and Enhanced Liver Fibrosis score.

265 ups, whereas significant changes in Enhanced Liver Fibrosis scores and liver stiffness were not obser

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

267 The identification of patients with advanced liver fibrosis secondary to non-alcoholic fatty liver di

268 Based on non-invasive tests for liver fibrosis, significant fibrosis was suspected in 20

269 ry or at release, no testing), treatment (if liver fibrosis stage >=F3, for all HCV infected or no tr

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

271 presence of HCC after adjusting for age and liver fibrosis stage, likely reflecting the downregulati

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

273 with the Pi*ZZ genotype, and increased with liver fibrosis stages.

274 Using non-invasive liver fibrosis tests (NILT) in primary care may permit e

275 ients had a higher prevalence of significant liver fibrosis than lean patients without NAFLD (15.7% v

276 ed nonalcoholic steatohepatitis and stage of liver fibrosis, the presence of rs738409 G/G genotype wa

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

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

279 ; however, it has not yet been evaluated for liver fibrosis treatment.

280 f AntiRetroviral Treatment (START) trial for liver fibrosis using the AST to Platelet Ratio Index (AP

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

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

283 nce imaging proton density fat fraction, and liver fibrosis was assessed by MRE-stiffness.

284 Liver fibrosis was assessed non-invasively via the serum

285 Significant liver fibrosis was defined as TE >=7.1 kPa.

286 tudy by magnetic resonance spectroscopy, and liver fibrosis was determined from a validated biomarker

287 Liver fibrosis was estimated by measuring liver stiffnes

288 Liver fibrosis was induced in these mice by administrati

289 Liver fibrosis was measured using the fibrosis 4 index (

290 Liver fibrosis was not observed by Masson staining and f

291 Conclusions: Significant liver fibrosis was rare among ART-naive HIV-positive per

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

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

294 mass/senescence, and inflammation as well as liver fibrosis were evaluated by both immunohistochemist

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

296 use severe inflammatory processes, including liver fibrosis, which is one of the most serious patholo

297 mary outcome was the change in the degree of liver fibrosis, which was presented as liver stiffness (

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

299 ur study identifies specific pathway driving liver fibrosis, with important diagnostic and therapeuti

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