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1 nd promoting sickness behaviors in mice with cholestatic liver injury.
2 1 could be potentially targeted to alleviate cholestatic liver injury.
3 L SR(-/-) mice, or Mdr2(-/-) mouse models of cholestatic liver injury.
4 irt1 presents a novel therapeutic target for cholestatic liver injury.
5 romised Sirt1 expression in rodent models of cholestatic liver injury.
6 ectin-3 regulates inflammasome activation in cholestatic liver injury.
7 ism and energy balance, but excess BAs cause cholestatic liver injury.
8 w summarizes present Kupffer cell studies in cholestatic liver injury.
9 potentially serve as an indicator of chronic cholestatic liver injury.
10 s and partial deficiencies in MDR3 result in cholestatic liver injury.
11 on is an effective strategy for ameliorating cholestatic liver injury.
12 otein 2 (MIP-2), which, in turn, exacerbates cholestatic liver injury.
13 TRAIL receptor signaling in a mouse model of cholestatic liver injury.
14 ed whether serotonin affects the severity of cholestatic liver injury.
15  of canalicular bile acid secretion leads to cholestatic liver injury.
16 ine bile duct ligation (BDL) model to induce cholestatic liver injury.
17 cal activation of Nrf2 may be beneficial for cholestatic liver injury.
18  bile secretion, and its deficiency leads to cholestatic liver injury.
19 ant NKT (iNKT) cells have been implicated in cholestatic liver injury.
20 role in the adaptive response to obstructive cholestatic liver injury.
21 fects on HGF activation critically influence cholestatic liver injury.
22 rhetinic acid (GA), in a hepatocyte model of cholestatic liver injury.
23 e of small cationic drugs may be impaired in cholestatic liver injury.
24 t in a variety of clinical settings leads to cholestatic liver injury.
25 c pathways is necessary to attenuate chronic cholestatic liver injury.
26  have been implicated in the pathogenesis of cholestatic liver injury.
27  is a well-established murine model to mimic cholestatic liver injury.
28 E2f2 deficiency conferred protection against cholestatic liver injury.
29 estrains DR cell expansion, thereby limiting cholestatic liver injury.
30 NLRP3 activation was analyzed in humans with cholestatic liver injury.
31 nt role of the UPR in the mechanism of human cholestatic liver injury.
32 plements have recently been shown to lead to cholestatic liver injury.
33 importance of the UPR in the pathogenesis of cholestatic liver injury.
34 omplete understanding of the pathogenesis of cholestatic liver injury.
35 +)TIM4(+) ResKCs were depleted after chronic cholestatic liver injury.
36 relationship with the progression from acute cholestatic liver injury (1 week) to the fully developed
37  In conclusion, neutrophils aggravated acute cholestatic liver injury after BDL.
38                        Neutrophils aggravate cholestatic liver injury after bile duct ligation (BDL).
39 been identified as an important mechanism of cholestatic liver injury and bile duct loss.
40 enteral nutrition (PN)-dependent may develop cholestatic liver injury and cirrhosis (PN-associated li
41 intestinal FXR dysfunction in a rat model of cholestatic liver injury and evaluated effects of obetic
42 ynthesis, thus preventing the development of cholestatic liver injury and fibrosis after bile duct li
43                                              Cholestatic liver injury and fibrosis were assessed by s
44 stigate the relevance of Fra-1 expression in cholestatic liver injury and fibrosis.
45      Ductular reactive (DR) cells exacerbate cholestatic liver injury and fibrosis.
46 le of the RBP, human antigen R (HuR), during cholestatic liver injury and hepatic stellate cell (HSC)
47 suggest that the loss of miR-194 ameliorates cholestatic liver injury and may suppress CYP7A1 express
48 the EGFR ligand, amphiregulin (AREG), during cholestatic liver injury and regulation of AREG expressi
49 hese findings highlight a role for STARD1 in cholestatic liver injury and suggest that its targeting
50 monstrates that reintroduction of MCs mimics cholestatic liver injury and that MC-derived TGF-B1 may
51 ne the extent and mechanisms of apoptosis in cholestatic liver injury and to explore the role of the
52                                              Cholestatic liver injury appears to result from the indu
53                      In two murine models of cholestatic liver injury, bile duct ligation (BDL) and a
54 sponse is crucial for bile acid (BA)-induced cholestatic liver injury, but molecular mechanisms remai
55 emodeling, we evaluated the role of PAI-1 in cholestatic liver injury by comparing the injury and rep
56 indings indicate that Kupffer cells abrogate cholestatic liver injury by cytokine-dependent mechanism
57 evated hepatic SLC35C1 expression attenuates cholestatic liver injury by enhancing CEACAM1 fucosylati
58 ulation of hydrophobic bile acids results in cholestatic liver injury by increasing oxidative stress,
59 ponents of the fibrinolytic pathway modulate cholestatic liver injury by regulating activation of hep
60                   MC injection recapitulates cholestatic liver injury characterized by increased DR,
61 erload critically drives the pathogenesis of cholestatic liver injury (CLI).
62 that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferat
63 3, with juvenile mice developing progressive cholestatic liver injury due to impaired biliary phospha
64  hepatic sarcoidosis, granulomas can cause a cholestatic liver injury, exemplified by elevated serum
65 (-/-) mice), a model of inflammation-induced cholestatic liver injury, fibrosis, and cancer.
66 y tract disorders culminating in progressive cholestatic liver injury, fibrosis, and often cirrhosis
67 sed by cells of the innate immune system, to cholestatic liver injury has not been explored.
68 a differential role during acute and chronic cholestatic liver injury in contrast to kidney injury.
69            SRT1720 administration alleviates cholestatic liver injury in mice by increasing hydrophil
70                                      Chronic cholestatic liver injury induced by cholestasis in roden
71 esses the hepatoprotective potential against cholestatic liver injury induced by hepatotoxin such as
72                   The effect of serotonin on cholestatic liver injury is not known.
73 cal roles in chronic tissue damage caused by cholestatic liver injury leading to fibrosis and cirrhos
74                                              Cholestatic liver injury leads to cell death and subsequ
75             This transcriptional response to cholestatic liver injury likely promotes partial de-diff
76 rvations support a pivotal role for TRAIL in cholestatic liver injury mediated by NK 1.1-positive NK/
77 iethoxycarbonyl-1,4-dihydrocollidine-feeding cholestatic liver injury model.
78      We have combined a mouse model of acute cholestatic liver injury, partial bile duct ligation (pB
79  role of the infiltrating neutrophils during cholestatic liver injury remains unclear.
80                                              Cholestatic liver injury results from the intrahepatic a
81 g the fibroproliferative response to chronic cholestatic liver injury, suggesting a role for Hh signa
82             PHB1 is an important mediator of cholestatic liver injury that regulates the activity of
83 employed a bile duct ligation (BDL) model of cholestatic liver injury to test the hypothesis that thi
84                                              Cholestatic liver injury was induced by bile duct ligati
85 his study, the biological role of miR-194 in cholestatic liver injury was investigated by using miR-1
86  the key role of Gal3 in the pathogenesis of cholestatic liver injury, we generated dnTGF-betaRII/gal
87      Moreover, murine models of fibrotic and cholestatic liver injury were used to demonstrate that t
88 onclusion, these findings support a model of cholestatic liver injury where Kupffer cell engulfment o
89 57BL/6 mice were exposed to DDC diet-induced cholestatic liver injury, which induced hepatomegaly and
90 ronic intestinal failure (CIF) often develop cholestatic liver injury, which may lead to liver failur