1 ied as hepatocellular (44%), mixed (28%), or
cholestatic (
28%).
2 nstream effector, was not implicated in cAMP
cholestatic action.
3 Interestingly, both choleretic and
cholestatic agents activate the same intracellular signa
4 Choleretic and
cholestatic agents affect bile formation, in part, by al
5 its expression is induced in the liver under
cholestatic and cirrhotic conditions.
6 82-96% of myofibroblasts in models of toxic,
cholestatic and fatty liver disease.
7 Using
cholestatic and hepatotoxic models of liver injury, we c
8 patocellular type and less frequently of the
cholestatic and mixed types.
9 iver injury (94% vs. 47%), which was usually
cholestatic and sometimes severe.
10 uated experimental fibrosis in the course of
cholestatic and toxic liver injury.
11 and nPKCdelta may be involved in choleretic,
cholestatic,
and anticholestatic effects by inserting, r
12 um BS levels, otherwise markedly elevated in
cholestatic animals.
13 st that pruritus and hyperalgesia in chronic
cholestatic BDL rats are associated with neuroinflammati
14 growth and secretin-stimulated choleresis in
cholestatic bile-duct-ligated (BDL) rats by interaction
15 ing supplements typically induce a prolonged
cholestatic but ultimately self-limiting liver injury th
16 y is specifically increased in patients with
cholestatic,
but not other forms of, systemic pruritus a
17 Moreover, severe
cholestatic complications and mortality after prolonged
18 In inflammatory
cholestatic conditions, loss of activity of liver AP (re
19 ROS levels, liver injury, and fibrosis under
cholestatic conditions.
20 rrhosis, intrahepatic cholestasis, and other
cholestatic conditions.
21 ead to more effective therapies for specific
cholestatic conditions.
22 e pathogenesis and treatment of a variety of
cholestatic conditions.
23 with Alagille syndrome, two major pediatric
cholestatic conditions.
24 is reduced in association with duct loss and
cholestatic destruction of nascent buds.
25 steroids is pertinent in the pathogenesis of
cholestatic disease and colon cancer.
26 eripheral blood of biliary atresia and other
cholestatic disease controls were characterized by fluor
27 Patients with
cholestatic disease exhibit pruritus and analgesia, but
28 ng cholangitis (PSC) is a rare, but serious,
cholestatic disease for which, to date, no effective the
29 Patients with
cholestatic disease have increased systemic concentratio
30 ecede cholestasis but may be of relevance to
cholestatic disease progression because altered fatty ac
31 tes with, and is the primary determinant of,
cholestatic disease severity in these patients.
32 ry sclerosing cholangitis (PSC) is a chronic
cholestatic disease that leads to extensive liver fibros
33 Primary sclerosing cholangitis is a chronic
cholestatic disease that may have an autoimmune basis.
34 dings were compared to children with genetic
cholestatic disease, age-matched deceased donor controls
35 rs: age, African-American race, hepatitis C,
cholestatic disease, body mass index >/= 35, pre-LT diab
36 oxicity is a major source of liver injury in
cholestatic disease, we explored the role of SHP in live
37 utants, whose symptoms cover the spectrum of
cholestatic disease.
38 d medicine for patients with ABCB4-dependent
cholestatic disease.
39 n of the once obscure inherited intrahepatic
cholestatic diseases of the liver, which, in turn, provi
40 Other
cholestatic diseases show similar activation, suggesting
41 ies of disease that will be reviewed include
cholestatic diseases, tumors, vascular anomalies, and ac
42 about the pathogenic mechanisms of specific
cholestatic diseases, which has limited our ability to m
43 Liver
cholestatic diseases, which stem from diverse etiologies
44 any missense mutations linked to less severe
cholestatic diseases.
45 h has led to novel therapies under study for
cholestatic diseases.
46 increase our understanding of these complex
cholestatic diseases.
47 nsive cells also occurred in other infantile
cholestatic diseases.
48 effective supplemental therapy with UDCA for
cholestatic diseases.
49 romising for functional PET of patients with
cholestatic diseases.
50 autoimmune cholangitis and potentially other
cholestatic diseases.
51 e putative role of liver AP in health and in
cholestatic diseases.
52 stasis of pregnancy, or hereditary pediatric
cholestatic disorders and may accompany, although less f
53 Most
cholestatic disorders are caused by defects in cholangio
54 Infantile
cholestatic disorders arise in the context of progressiv
55 ts compared to patients with other infantile
cholestatic disorders, thereby establishing a possible e
56 d Drug Administration-approved treatment for
cholestatic disorders.
57 might help us to better understand and treat
cholestatic disorders.
58 in intrahepatic bile ducts of patients with
cholestatic disorders.
59 rosetting of hepatocytes, consistent with a
cholestatic drug reaction.
60 This first-in-class study evaluated the anti-
cholestatic effects and safety of seladelpar in patients
61 plasma membrane, and nPKCepsilon may mediate
cholestatic effects by retrieving MRP2 from the plasma m
62 An emerging theme is that choleretic and
cholestatic effects may be mediated by different isoform
63 discriminate between IAC and the more common
cholestatic entities, primary (PSC) and secondary sclero
64 % chronic, 7% acute on chronic, and 6% acute
cholestatic failure.
65 sting, as well as in plasma samples from six
cholestatic gene knockout mice and six age- and gender-m
66 d male with HCV genotype 1b developed severe
cholestatic HCV at 6 months posttransplant with ascites,
67 cute (9%) and chronic cholestasis (10%), and
cholestatic hepatitis (29%).
68 e patients with advanced fibrosis and 9 with
cholestatic hepatitis (74% men, 57% genotype 1a, 63% pre
69 hepatitis C, including those with fibrosing
cholestatic hepatitis (FCH) and decompensated cirrhosis
70 All five patients with fibrosing
cholestatic hepatitis achieved SVR12 (100%, 90% CI 55-10
71 Nine patients presented with
cholestatic hepatitis and 12 patients presented with hep
72 (Mdr2-KO) mice spontaneously develop chronic
cholestatic hepatitis and fibrosis that is eventually fo
73 inflammation-mediated HCC, develops chronic
cholestatic hepatitis at an early age and HCC at an adul
74 Bile duct loss during acute
cholestatic hepatitis is an ominous early indicator of p
75 type 1 HCV and advanced fibrosis (F3-4/4) or
cholestatic hepatitis treated with telaprevir- or bocepr
76 me with growth failure or transient neonatal
cholestatic hepatitis.
77 he most common clinical pattern was a severe
cholestatic hepatitis.
78 P-A, CTP-B, or CTP-C cirrhosis; or fibrosing
cholestatic hepatitis.
79 d in 51% with advanced fibrosis and 44% with
cholestatic hepatitis.
80 d in 22% with advanced fibrosis and 33% with
cholestatic hepatitis.
81 irment, and by all 6 patients with fibrosing
cholestatic hepatitis.
82 hepatic impairment; and those with fibrosing
cholestatic hepatitis.
83 those with advanced fibrosis (F3-F4) and/or
cholestatic hepatitis.
84 atients with recurrent advanced fibrosis and
cholestatic hepatitis.
85 Twenty-seven percent had fibrosing
cholestatic hepatitis/early aggressive HCV in the graft,
86 PDH and nitrosylated HDAC2 were increased in
cholestatic human and rat livers reflecting increased co
87 ere tested in cholangiocytes from normal and
cholestatic human livers.
88 obstruction results in a well-characterized
cholestatic inflammatory and fibrogenic process; however
89 suggesting that this is a common response to
cholestatic injury in infancy.
90 ration and prevents parenchymal damage after
cholestatic injury in mice and thus may mediate the resp
91 Although
cholestatic injury is common to many forms of liver dise
92 of Mrp4 in a protective adaptive response to
cholestatic injury is not known.
93 genesis of liver fibrosis development in the
cholestatic injury model, for HSC activation, and for th
94 onversely, histology of the 73 patients with
cholestatic injury more often demonstrated bile plugs an
95 dergoes adaptive upregulation in response to
cholestatic injury or bile acid feeding.
96 Cholestatic injury precedes liver fibrosis, and cholangi
97 judged to become chronic, with drugs causing
cholestatic injury predominating.
98 mechanisms regulating liver repair following
cholestatic injury remain largely unknown.
99 Cholestatic injury was associated with female gender and
100 e treated mice suffering from a steatotic or
cholestatic injury with anti-TNF-alpha antibodies (Infli
101 or older (n = 149) were more likely to have
cholestatic injury, although mortality and rate of liver
102 ticipates in the regenerative response after
cholestatic injury.
103 ular reaction, which are repair responses to
cholestatic injury.
104 The most common causes of
cholestatic jaundice are biliary atresia and idiopathic
105 uld be aware that ajmaline may induce severe
cholestatic jaundice even after a single dose administra
106 is preceded by hepatic complications such as
cholestatic jaundice or hepatomegaly.
107 NICCD and non-NICCD, infants with idiopathic
cholestatic jaundice or INH were enrolled.
108 hree weeks later, he presented with painless
cholestatic jaundice which peaked in severity at eleven
109 <16.3) but there were no clinical signs of
cholestatic jaundice, pruritis, or liver dysfunction.
110 hondrial antibody-positive titer >/=1 in 40,
cholestatic liver blood tests, diagnostic or compatible
111 eactive oxygen species that might exacerbate
cholestatic liver damage.
112 flammatory response and neutrophil-dependent
cholestatic liver damage.
113 in validation cohorts) and in controls with
cholestatic liver disease (n = 44).
114 tion, PCN risk was higher in recipients with
cholestatic liver disease (SIR 2.78); five of these case
115 ur cohort of 28 MVID patients, 8 developed a
cholestatic liver disease akin to progressive familial i
116 -alcoholic steatohepatitis, viral hepatitis,
cholestatic liver disease and autoimmune liver diseases.
117 or future pharmacological strategies against
cholestatic liver disease and cancer.
118 ulation of bile acid homeostasis can lead to
cholestatic liver disease and endoplasmic reticulum (ER)
119 e composition with important applications in
cholestatic liver disease and gallstone disease, two ser
120 ry sclerosing cholangitis (PSC) is a chronic
cholestatic liver disease and one of the most common ind
121 Primary biliary cirrhosis is a chronic
cholestatic liver disease characterised by destruction o
122 Primary sclerosing cholangitis is a chronic
cholestatic liver disease characterized by strictures of
123 Primary sclerosing cholangitis is a chronic
cholestatic liver disease characterized by strictures of
124 Primary sclerosing cholangitis is a chronic
cholestatic liver disease characterized by strictures of
125 y the ABCB11 gene, causes severe progressive
cholestatic liver disease from early infancy.
126 centers with either autoimmune hepatitis or
cholestatic liver disease had significantly lower risks
127 Recent advances in
cholestatic liver disease have occurred in several areas
128 r plasminogen activator inhibitor (PAI)-1 in
cholestatic liver disease in mice suggested that tissue-
129 sm contribute to the pathogenesis of chronic
cholestatic liver disease in mice.
130 ibute to the pathogenesis and progression of
cholestatic liver disease in mice.
131 eased awareness of PBC as a cause of chronic
cholestatic liver disease is critical in evaluating non-
132 with primary biliary cirrhosis, an important
cholestatic liver disease of adults.
133 Primary sclerosing cholangitis is a chronic
cholestatic liver disease of unknown etiology.
134 ic bile duct development and their effect on
cholestatic liver disease phenotypes.
135 urthermore, nicotine may act as a mitogen in
cholestatic liver disease processes, thereby facilitatin
136 1950s as a clinical syndrome of progressive
cholestatic liver disease resulting from chronic inflamm
137 , 25% of patients undergoing OLT for chronic
cholestatic liver disease still develop de novo fracture
138 liary cirrhosis (PBC) is an uncommon chronic
cholestatic liver disease that primarily afflicts young
139 ry sclerosing cholangitis (PSC) is a chronic
cholestatic liver disease that progresses to death as a
140 We used a mouse model of
cholestatic liver disease to investigate mechanisms of i
141 malabsorption syndromes (especially owing to
cholestatic liver disease), antibiotic therapy, and rena
142 infants transplanted for reasons other than
cholestatic liver disease, and patients transplanted bet
143 dents is often studied as an animal model of
cholestatic liver disease, characterized by obstruction
144 UDCA, a bile acid used in the treatment of
cholestatic liver disease, has anti-inflammatory and cyt
145 alidity of risk stratification in autoimmune
cholestatic liver disease, highlighting strengths and we
146 During
cholestatic liver disease, there is dysregulation in the
147 an age at LTx was 9 months, the majority had
cholestatic liver disease, were hospitalized pre-LTx, an
148 neficial use of fenofibrate therapy in human
cholestatic liver disease.
149 itochondrial morphology has been observed in
cholestatic liver disease.
150 tight-junction structure, leading to severe
cholestatic liver disease.
151 ochondrial morphology to the pathogenesis of
cholestatic liver disease.
152 , MDR3 is a potential therapeutic target for
cholestatic liver disease.
153 d (TUDC), is a mainstay for the treatment of
cholestatic liver disease.
154 ndings from genetic studies of patients with
cholestatic liver disease.
155 the formation of bile and the prevention of
cholestatic liver disease.
156 were increased in livers from patients with
cholestatic liver disease.
157 n the liver and prevent hepatocyte injury in
cholestatic liver disease.
158 g colon cancer formation and progression and
cholestatic liver disease.
159 fusion (IR) injury is frequently followed by
cholestatic liver disease.
160 rine when hepatic elimination is impaired by
cholestatic liver disease.
161 ted here suggest that PHB1 is also linked to
cholestatic liver disease.
162 which is frequently used in the treatment of
cholestatic liver disease.
163 ocrine phenotypes of cholangiocytes in human
cholestatic liver diseases (ie, cholangiopathies) that a
164 langiocytes occurs during the progression of
cholestatic liver diseases and is critical for the maint
165 igands may ameliorate human diseases such as
cholestatic liver diseases and the associating acute ren
166 epidemiology, and treatment of a variety of
cholestatic liver diseases and their associated complica
167 Cholestatic liver diseases are caused by a range of hepa
168 Human chronic
cholestatic liver diseases are characterized by cholangi
169 target of cholangiopathies that are chronic
cholestatic liver diseases characterized by loss of prol
170 a modifier gene in patients with concurrent
cholestatic liver diseases such as cystic fibrosis.
171 ymptom commonly experienced by patients with
cholestatic liver diseases such as primary biliary chola
172 ruritus is a common symptom in patients with
cholestatic liver diseases such as primary biliary cirrh
173 but is believed to play an important role in
cholestatic liver diseases such as primary familial intr
174 peutic indications in constipation, dry eye,
cholestatic liver diseases, and inflammatory lung disord
175 ression of many of these genes is altered in
cholestatic liver diseases, but few have been extensivel
176 advances have been made in the treatment of
cholestatic liver diseases, including primary biliary ci
177 During the course of
cholestatic liver diseases, mitotically dormant cholangi
178 In this review we develop the argument that
cholestatic liver diseases, particularly primary biliary
179 cholangitis (PSC) are infrequent autoimmune
cholestatic liver diseases, that disproportionate to the
180 e for the maintenance of biliary mass during
cholestatic liver diseases.
181 itus and painless jaundice that occur during
cholestatic liver diseases.
182 ial targets for pharmacological therapies of
cholestatic liver diseases.
183 r (FXR) and its potential therapeutic use in
cholestatic liver diseases.
184 beticholic acid for the treatment of chronic
cholestatic liver diseases.
185 gies targeting BA transport and signaling in
cholestatic liver diseases.
186 DHEA-S levels was not seen in patients with
cholestatic liver diseases.
187 et to modulate bile flow in the treatment of
cholestatic liver diseases.
188 his review focuses on the recent advances in
cholestatic liver diseases.
189 frequently the most debilitating symptom of
cholestatic liver diseases.
190 dvance our understanding of the treatment of
cholestatic liver diseases.
191 better understanding of the pathogenesis of
cholestatic liver diseases.
192 better understanding of the pathogenesis of
cholestatic liver diseases.
193 biting PAI-1 might attenuate liver injury in
cholestatic liver diseases.
194 ary cholangitis (PBC) pathogenesis and other
cholestatic liver diseases.
195 aling may be important for the management of
cholestatic liver diseases.
196 rters and are natural targets for therapy of
cholestatic liver diseases.
197 ry sclerosing cholangitis (PSC) is a chronic
cholestatic liver disorder characterized by inflammation
198 Primary biliary cirrhosis (PBC) is a chronic
cholestatic liver disorder that can progress to cirrhosi
199 eriously disabling symptom accompanying many
cholestatic liver disorders.
200 modulate bile formation in the treatment of
cholestatic liver disorders.
201 and therapy, such as fenofibrate, in various
cholestatic liver disorders.
202 y gastrointestinal diseases, including human
cholestatic liver disorders.
203 Cholestatic liver dysfunction (CLD) and biliary sludge o
204 s acute, chronic, acute-on-chronic, or acute
cholestatic liver failure.
205 Liver specimens from patients with
cholestatic liver fibrosis had increased numbers of MSLN
206 In addition,
cholestatic liver fibrosis induced by BDL, as determined
207 RA treatment in mice with existing
cholestatic liver fibrosis inhibits HSC activation and p
208 Cholestatic liver fibrosis is caused by obstruction of t
209 ike inhibitor of differentiation 1 (EID1) in
cholestatic liver fibrosis.
210 e, enteric TNFRI is an important mediator of
cholestatic liver fibrosis.
211 been identified as an important mechanism of
cholestatic liver injury and bile duct loss.
212 enteral nutrition (PN)-dependent may develop
cholestatic liver injury and cirrhosis (PN-associated li
213 intestinal FXR dysfunction in a rat model of
cholestatic liver injury and evaluated effects of obetic
214 stigate the relevance of Fra-1 expression in
cholestatic liver injury and fibrosis.
215 le of the RBP, human antigen R (HuR), during
cholestatic liver injury and hepatic stellate cell (HSC)
216 indings indicate that Kupffer cells abrogate
cholestatic liver injury by cytokine-dependent mechanism
217 ponents of the fibrinolytic pathway modulate
cholestatic liver injury by regulating activation of hep
218 sed by cells of the innate immune system, to
cholestatic liver injury has not been explored.
219 SRT1720 administration alleviates
cholestatic liver injury in mice by increasing hydrophil
220 Chronic
cholestatic liver injury induced by cholestasis in roden
221 esses the hepatoprotective potential against
cholestatic liver injury induced by hepatotoxin such as
222 The effect of serotonin on
cholestatic liver injury is not known.
223 This transcriptional response to
cholestatic liver injury likely promotes partial de-diff
224 rvations support a pivotal role for TRAIL in
cholestatic liver injury mediated by NK 1.1-positive NK/
225 iethoxycarbonyl-1,4-dihydrocollidine-feeding
cholestatic liver injury model.
226 PHB1 is an important mediator of
cholestatic liver injury that regulates the activity of
227 Moreover, murine models of fibrotic and
cholestatic liver injury were used to demonstrate that t
228 (-/-) mice), a model of inflammation-induced
cholestatic liver injury, fibrosis, and cancer.
229 We have combined a mouse model of acute
cholestatic liver injury, partial bile duct ligation (pB
230 g the fibroproliferative response to chronic
cholestatic liver injury, suggesting a role for Hh signa
231 the key role of Gal3 in the pathogenesis of
cholestatic liver injury, we generated dnTGF-betaRII/gal
232 nd promoting sickness behaviors in mice with
cholestatic liver injury.
233 s and partial deficiencies in MDR3 result in
cholestatic liver injury.
234 on is an effective strategy for ameliorating
cholestatic liver injury.
235 otein 2 (MIP-2), which, in turn, exacerbates
cholestatic liver injury.
236 ed whether serotonin affects the severity of
cholestatic liver injury.
237 of canalicular bile acid secretion leads to
cholestatic liver injury.
238 ine bile duct ligation (BDL) model to induce
cholestatic liver injury.
239 cal activation of Nrf2 may be beneficial for
cholestatic liver injury.
240 bile secretion, and its deficiency leads to
cholestatic liver injury.
241 ant NKT (iNKT) cells have been implicated in
cholestatic liver injury.
242 role in the adaptive response to obstructive
cholestatic liver injury.
243 fects on HGF activation critically influence
cholestatic liver injury.
244 1 could be potentially targeted to alleviate
cholestatic liver injury.
245 L SR(-/-) mice, or Mdr2(-/-) mouse models of
cholestatic liver injury.
246 irt1 presents a novel therapeutic target for
cholestatic liver injury.
247 romised Sirt1 expression in rodent models of
cholestatic liver injury.
248 ectin-3 regulates inflammasome activation in
cholestatic liver injury.
249 w summarizes present Kupffer cell studies in
cholestatic liver injury.
250 potentially serve as an indicator of chronic
cholestatic liver injury.
251 that lipid metabolism contributed to chronic
cholestatic liver injury; crossing peroxisome proliferat
252 range of potentially valuable actions on the
cholestatic liver, has not yet been proved to make a sub
253 d to effectively extrude bile acids from the
cholestatic liver.
254 contributes to accelerating fibrogenesis in
cholestatic livers by mediating the initial inflammation
255 not produce FGF19, nonparenchymal cells from
cholestatic livers produce FGF19.
256 n was tested in cholangiocytes of normal and
cholestatic livers.
257 kout mice, as well as in myrcludex B-treated
cholestatic mice, whereas plasma FGF19 was not induced i
258 -regulation of ATP11C protein in livers from
cholestatic mice, which coincided with reduced OATP1B2 l
259 cluding 19 hepatocellular injury (HC) and 16
cholestatic/
mixed injury (CS)] and AIH (n = 28) were eva
260 er disease, ischemia/reperfusion injury, and
cholestatic models of liver disease.
261 Females from
cholestatic mothers developed a severe obese, diabetic p
262 b treatment, at least in these steatotic and
cholestatic mouse models, is the safer approach since it
263 nalysis, cotrimoxazole was associated with a
cholestatic or ductopenic injury (OR = 7.05 [2.50-19.89]
264 After UDCA removal
cholestatic parameters, taurine species of cholic acid a
265 iary insults, these mice exhibit exacerbated
cholestatic pathologies.
266 ong-sought pruritogenic signaling cascade in
cholestatic patients suffering from itch.
267 Ten
cholestatic patients were identified as vitamin A-defici
268 provide evidence for renal tubular injury in
cholestatic patients with cholemic nephropathy.
269 ption lower the BS load and are best used in
cholestatic patients.
270 is more common in younger patients, whereas
cholestatic pattern increases with older age.
271 A
cholestatic pattern was found in 60.0% of patients and w
272 In this study, we show that the
cholestatic phenotype induced by common bile duct ligati
273 Our data demonstrate that the
cholestatic potential of certain drugs may be aggravated
274 elieve this is the first report showing that
cholestatic pregnancy in the absence of altered maternal
275 ased transplacental cholesterol transport in
cholestatic pregnancy.
276 ocesses, including vasculogenesis, fibrosis,
cholestatic pruritus and tumour progression.
277 s, including cancer, fibrosis, inflammation,
cholestatic pruritus, and pain.
278 enesis, neuropathic pain, fibrotic diseases,
cholestatic pruritus, lymphocyte homing, and thrombotic
279 s TRPA1, might be developed for treatment of
cholestatic pruritus.
280 rvating the skin is thought to contribute to
cholestatic pruritus.
281 atidic acid (LPA), as potential mediators of
cholestatic pruritus.
282 sertraline and to evaluate its efficacy for
cholestatic pruritus.
283 ve and mechanistic research in patients with
cholestatic pruritus.
284 PDH nitrosylation was assessed in normal and
cholestatic rat and human livers.
285 he liver of 17alpha-ethinylestradiol-induced
cholestatic rats improves bile flow, in part by enhancin
286 AdhAQP1-transduced
cholestatic rats increased the biliary output of major e
287 In AdhAQP1-transduced
cholestatic rats, BSEP showed a canalicular microdomain
288 a, 30% METAVIR F3-F4, 4% decompensation, 11%
cholestatic recurrence, 7% had kidney transplant, and 82
289 alpha and beta isoforms exhibited heightened
cholestatic sensitivity.
290 e regulation of bile formation in normal and
cholestatic states and greater insight into the pathogen
291 Testing the chip on subjects with
cholestatic syndromes identified disease-causing mutatio
292 ns of transporter genes can cause hereditary
cholestatic syndromes in both infants and adults as well
293 w insights into the pathogenesis of specific
cholestatic syndromes including primary biliary cirrhosi
294 iver samples from individuals with different
cholestatic syndromes, suggesting that reduced FOXA2 abu
295 ns of transporter genes can cause hereditary
cholestatic syndromes, the study of which has shed much
296 rthered our understanding of cholestasis and
cholestatic syndromes.
297 e molecular basis of hereditary and acquired
cholestatic syndromes.
298 Recent studies have identified a
cholestatic variant of nonalcoholic fatty liver disease
299 Adult livers were severely
cholestatic,
with levels of bile salts >1 mM, but no evi
300 iver enzymes were significantly increased in
cholestatic WT mice and significantly blunted in TRPC5 K