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1 ectin-3 regulates inflammasome activation in cholestatic liver injury.
2 w summarizes present Kupffer cell studies in cholestatic liver injury.
3 potentially serve as an indicator of chronic cholestatic liver injury.
4 s and partial deficiencies in MDR3 result in cholestatic liver injury.
5 on is an effective strategy for ameliorating cholestatic liver injury.
6 nd promoting sickness behaviors in mice with cholestatic liver injury.
7 otein 2 (MIP-2), which, in turn, exacerbates cholestatic liver injury.
8 ed whether serotonin affects the severity of cholestatic liver injury.
9 of canalicular bile acid secretion leads to cholestatic liver injury.
10 ine bile duct ligation (BDL) model to induce cholestatic liver injury.
11 cal activation of Nrf2 may be beneficial for cholestatic liver injury.
12 bile secretion, and its deficiency leads to cholestatic liver injury.
13 ant NKT (iNKT) cells have been implicated in cholestatic liver injury.
14 role in the adaptive response to obstructive cholestatic liver injury.
15 fects on HGF activation critically influence cholestatic liver injury.
16 rhetinic acid (GA), in a hepatocyte model of cholestatic liver injury.
17 e of small cationic drugs may be impaired in cholestatic liver injury.
18 t in a variety of clinical settings leads to cholestatic liver injury.
19 c pathways is necessary to attenuate chronic cholestatic liver injury.
20 have been implicated in the pathogenesis of cholestatic liver injury.
21 1 could be potentially targeted to alleviate cholestatic liver injury.
22 L SR(-/-) mice, or Mdr2(-/-) mouse models of cholestatic liver injury.
23 irt1 presents a novel therapeutic target for cholestatic liver injury.
24 romised Sirt1 expression in rodent models of cholestatic liver injury.
25 relationship with the progression from acute cholestatic liver injury (1 week) to the fully developed
29 enteral nutrition (PN)-dependent may develop cholestatic liver injury and cirrhosis (PN-associated li
30 intestinal FXR dysfunction in a rat model of cholestatic liver injury and evaluated effects of obetic
32 le of the RBP, human antigen R (HuR), during cholestatic liver injury and hepatic stellate cell (HSC)
33 ne the extent and mechanisms of apoptosis in cholestatic liver injury and to explore the role of the
35 emodeling, we evaluated the role of PAI-1 in cholestatic liver injury by comparing the injury and rep
36 indings indicate that Kupffer cells abrogate cholestatic liver injury by cytokine-dependent mechanism
37 ulation of hydrophobic bile acids results in cholestatic liver injury by increasing oxidative stress,
38 ponents of the fibrinolytic pathway modulate cholestatic liver injury by regulating activation of hep
39 that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferat
44 esses the hepatoprotective potential against cholestatic liver injury induced by hepatotoxin such as
47 rvations support a pivotal role for TRAIL in cholestatic liver injury mediated by NK 1.1-positive NK/
52 g the fibroproliferative response to chronic cholestatic liver injury, suggesting a role for Hh signa
54 employed a bile duct ligation (BDL) model of cholestatic liver injury to test the hypothesis that thi
56 the key role of Gal3 in the pathogenesis of cholestatic liver injury, we generated dnTGF-betaRII/gal
58 onclusion, these findings support a model of cholestatic liver injury where Kupffer cell engulfment o
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