ライフサイエンスコーパス: liver regeneration

1 e role of natural killer T cells in impaired liver regeneration.

2 FR) are critically involved in initiation of liver regeneration.

3 atalytic activity during the early stages of liver regeneration.

4 y regulating the TNFalpha/HB-EGF axis during liver regeneration.

5 adult liver progenitors that participate in liver regeneration.

6 ion of various metabolic pathways as well as liver regeneration.

7 nd that specific deletion of Fak accelerates liver regeneration.

8 ors we investigated the role of SOCS2 during liver regeneration.

9 cretion, elevated liver injury, and impaired liver regeneration.

10 The rat is an important model for liver regeneration.

11 ated the steatosis that normally accompanies liver regeneration.

12 chanisms that are involved in termination of liver regeneration.

13 echanism may contribute to platelet-mediated liver regeneration.

14 K) signaling, which critically contribute to liver regeneration.

15 ocytes, and this cross-talk may occur during liver regeneration.

16 we reported on a key role for MMP10 in mouse liver regeneration.

17 also accumulate in the liver during impaired liver regeneration.

18 lesterol uptake into hepatocytes and affects liver regeneration.

19 with anti CD1d antibodies exhibited reduced liver regeneration.

20 multiple effects fine-tuning the kinetics of liver regeneration.

21 shed the alpha-GalCer-mediated inhibition of liver regeneration.

22 oxification (Sult2a1) leading to an improved liver regeneration.

23 tion and liver marker gene expression during liver regeneration.

24 as regulated during and essential for normal liver regeneration.

25 some recover spontaneously and show complete liver regeneration.

26 tant for adult organ growth, as it modulates liver regeneration.

27 ism, nonalcoholic liver disease (NAFLD), and liver regeneration.

28 ns for the understanding and manipulation of liver regeneration.

29 therapy in a porcine model of cirrhosis for liver regeneration.

30 differentiate to hepatocytes contributing to liver regeneration.

31 production by iNKT cells, markedly inhibited liver regeneration.

32 h aberrant healing (fibrosis) that overrides liver regeneration.

33 inhibiting bacterial infection and promoting liver regeneration.

34 developed extensive liver injury and robust liver regeneration.

35 her E-cyclin or Cdk2 does not affect overall liver regeneration.

36 and IFN-gamma production, thereby inhibiting liver regeneration.

37 of TRAS-derived lipids to fuel hypertrophic liver regeneration.

38 multiple effects fine-tuning the kinetics of liver regeneration.

39 MSCs as important players in stem cell-based liver regeneration.

40 AR-4 blockade did not suppress hemostasis or liver regeneration.

41 (-/-) and Jalpha281(-/-) mice, showed normal liver regeneration.

42 totally reversed the observed attenuation of liver regeneration.

43 partial hepatectomy (PHx) was used to study liver regeneration.

44 ted the inhibitory effect of alpha-GalCer on liver regeneration.

45 vated CCl4 -induced liver injury and impeded liver regeneration.

46 ATP elevates NK cell cytotoxicity and boosts liver regeneration.

47 to rapid S-phase entry of hepatocytes during liver regeneration.

48 performed for genes known to be involved in liver regeneration.

49 lure by preventing apoptosis and by inducing liver regeneration.

50 uction of liver apoptosis and enhancement of liver regeneration.

51 ed to better define the role of Casp8 during liver regeneration.

52 iated cell signaling has been shown to boost liver regeneration.

53 tes facilitates hepatocyte proliferation and liver regeneration.

54 le of Nogo-B in hepatocyte proliferation and liver regeneration.

55 and liver) and impairs sperm development and liver regeneration.

56 e cells, which regulate and ultimately drive liver regeneration.

57 ts fibrogenic response and augments fibrotic liver regeneration.

58 s unique LT setting, as an exemplar of human liver regeneration.

59 of molecular processes associated with human liver regeneration.

60 o the liver, rather than mature LSECs, drive liver regeneration.

61 feration, providing novel clues for enhanced liver regeneration.

62 r (NK) cell-mediated purinergic signaling on liver regeneration.

63 f the acute phase response and regulation of liver regeneration.

64 stem cells and their derived hepatocytes for liver regeneration.

65 fter APAP overdose is associated with timely liver regeneration.

66 for the complement-induced priming phase of liver regeneration.

67 ic properties of hepatocytes with respect to liver regeneration.

68 Oxygen is a key regulator of liver regeneration.

69 latelets within the liver after induction of liver regeneration.

70 d quantitative insights into the dynamics of liver regeneration.

71 endothelial cell-hepatocyte crosstalk during liver regeneration.

72 rograms with potential applications to adult liver regeneration.

73 ntrol morphogenic signaling during effective liver regeneration.

74 and little is known about its role in adult liver regeneration.

75 During liver regeneration, a clone of hepatocytes that expresse

76 ted ISC/export pathway in which augmenter of liver regeneration, a mitochondrial Mia40-dependent prot

77 treated with terlipressin had an increase in liver regeneration after 30% PH and increased survival a

78 Knockdown of ANLN did not affect liver regeneration after acute and chronic liver injurie

79 s illuminate a previously unknown program of liver regeneration after acute injury and allow for expl

80 Timely initiation of compensatory liver regeneration after APAP hepatotoxicity is critical

81 role of glycogen synthase kinase 3 (GSK3) in liver regeneration after APAP hepatotoxicity using a pha

82 ential role of several signaling pathways in liver regeneration after APAP overdose and highlighted c

83 r study has revealed a novel role of GSK3 in liver regeneration after APAP overdose and identified GS

84 aspartic acid, in mice resulted in improved liver regeneration after APAP overdose.

85 Liver regeneration after APAP treatment was significantl

86 ion of liver injury and significantly higher liver regeneration after APAP treatment.

87 ntified major signaling pathways involved in liver regeneration after APAP-induced acute liver injury

88 al for final recovery, but the mechanisms of liver regeneration after APAP-induced ALF have not been

89 as a potential therapeutic target to improve liver regeneration after APAP-induced ALF.

90 ase, is involved in this process, we studied liver regeneration after carbon tetrachloride (CCl4) adm

91 Various mouse models of liver regeneration after extended partial hepatectomy an

92 Various mouse models of liver regeneration after extended partial hepatectomy an

93 ameliorated hepatic dysfunction and improved liver regeneration after extended resection by paracrine

94 ceptor 1 (Nor-1) and its target genes during liver regeneration after hepatectomy in mice, and in hep

95 iated by cytokine secretion is essential for liver regeneration after hepatic resection, yet the mech

96 pression of LSP1 in mouse hepatocytes during liver regeneration after injection of an LSP1 expression

97 LSECs) have long been noted to contribute to liver regeneration after liver injury.

98 ll-directed therapy may significantly affect liver regeneration after liver resection or transplantat

99 srupting Hedgehog signaling in MFs inhibited liver regeneration after partial hepactectomy (PH).

100 e contribution of CcnE1, CcnE2, and Cdk2 for liver regeneration after partial hepatectomy (PH) by gen

101 BACKGROUND & AIMS: Liver regeneration after partial hepatectomy (PH) increa

102 Many regulatory pathways are involved in liver regeneration after partial hepatectomy (PH) to ini

103 Many regulatory pathways are involved in liver regeneration after partial hepatectomy (PH), to in

104 ver lymphocytes and parenchymal cells during liver regeneration after partial hepatectomy (PH).

105 Moreover, liver regeneration after partial hepatectomy also depend

106 EDHB selectively augmented liver regeneration after partial hepatectomy and portal

107 EDHB selectively augmented liver regeneration after partial hepatectomy and portal

108 demonstrate here that eosinophils stimulate liver regeneration after partial hepatectomy and toxin-m

109 We used liver regeneration after partial hepatectomy as a physio

110 nd PHD3) is a suitable strategy to stimulate liver regeneration after partial hepatectomy for colorec

111 nd PHD3) is a suitable strategy to stimulate liver regeneration after partial hepatectomy for colorec

112 ate the effect of 5-HT7 receptor blockade on liver regeneration after partial hepatectomy.

113 the late priming and proliferative phases of liver regeneration after partial hepatectomy.

114 post-PH by the use of terlipressin improves liver regeneration after PH in lean and steatotic mouse

115 ntially reduced hepatocyte proliferation and liver regeneration after PH in vivo.

116 During liver regeneration after PH, P2X4 contributes to the com

117 iNKT cells play a minor role in controlling liver regeneration after PHx under healthy conditions.

118 mesenteric lymph nodes and exhibited reduced liver regeneration after PHx.

119 proteins is essential for the termination of liver regeneration after surgery and for maintenance of

120 livers of C/EBPalpha-S193A mice fail to stop liver regeneration after surgery when livers reach the o

121 al PHD inhibition on tumor expansion, and on liver regeneration after surgical resection.

122 al PHD inhibition on tumor expansion, and on liver regeneration after surgical resection.

123 generate an animal model that fails to stop liver regeneration after surgical resections and elucida

124 und that Fak is activated and induced during liver regeneration after two-thirds partial hepatectomy

125 e Mia40, the sulfhydryl oxidase augmenter of liver regeneration (ALR), and the intracellular glutathi

126 idues in the sulfhydryl oxidase augmenter of liver regeneration (ALR).

127 Augmenter of liver regeneration (ALR, encoded by GFER) is a widely di

128 n blood and bile after PH and contributes to liver regeneration, although purinergic receptors and me

129 normal and pathological conditions, such as liver regeneration and cancer.

130 s critical during the initial phases of both liver regeneration and carcinogenesis and provide key me

131 -) were used to explore whether AhR controls liver regeneration and carcinogenesis by restricting the

132 s of DRs and their potential contribution to liver regeneration and carcinogenesis.

133 get for therapeutic interventions to improve liver regeneration and clinical outcomes after partial h

134 el mechanism of action of beta1-integrins in liver regeneration and demonstrate that protein depletio

135 velopment and bile duct formation as well as liver regeneration and disease.

136 tion, Hoip(Deltahep) mice displayed enhanced liver regeneration and DNA damage.

137 TCS-mediated liver regeneration and fibrosis preceded HCC development

138 of ADAM17 substrates, which are pivotal for liver regeneration and function.

139 tissues and cells; we examined its roles in liver regeneration and HCC proliferation.

140 Unexpectedly, however, liver regeneration and hepatocarcinogenesis was impaired

141 growth factor receptor (EGFR) pathway during liver regeneration and hepatocarcinogenesis.

142 triggered by hepatocyte loss is required for liver regeneration and maintenance but also promotes dev

143 nk between cell proliferative effects during liver regeneration and metabolic regulation of FXR was e

144 ibitor ethyl-3,4-dihydroxybenzoate (EDHB) on liver regeneration and metastatic tumor growth.

145 ibitor ethyl-3,4-dihydroxybenzoate (EDHB) on liver regeneration and metastatic tumor growth.

146 miR-122, miR-21, and miR-221 are involved in liver regeneration and might contribute to spontaneous r

147 diseased liver may be regulated to optimize liver regeneration and minimize the likelihood of tumori

148 information regarding the mechanisms behind liver regeneration and possibilities to inhibit dediffer

149 to mice treated with NR, exhibited enhanced liver regeneration and reduced steatosis following parti

150 the data in support of a metabolic model of liver regeneration and reflects on the clinical implicat

151 ocellular carcinoma, but its contribution to liver regeneration and repair in acute liver injury are

152 PCs are thought to play an important role in liver regeneration and repair responses.

153 he pursuit of A20-based therapies to promote liver regeneration and repair.

154 tified process of ammonia consumption during liver regeneration and revealed unexpected concomitant c

155 ans-signaling has been linked to accelerated liver regeneration and several chronic inflammatory path

156 cell-derived IL-22 is required for efficient liver regeneration and that secretion of IL-22 in the re

157 ess, the most proximal events that stimulate liver regeneration and the distal signals that terminate

158 -scale proteomics to identify key players in liver regeneration and the importance of posttranslation

159 l killer T cells is markedly elevated during liver regeneration and their activation under different

160 of major growth factor receptors involved in liver regeneration and their downstream mitogenic signal

161 h of p21 activation determine its effects on liver regeneration and tumor development in the liver.

162 chromatin compaction in cultured cells, and liver regeneration and tumor formation in mice.

163 tly controlled replication of hepatocytes in liver regeneration and uncontrolled proliferation of tum

164 This slowed liver regeneration and was associated with reduced expre

165 uction of IFN-gamma, which directly inhibits liver regeneration, and IL-4, which indirectly attenuate

166 ggest that Fak is involved in the process of liver regeneration, and inhibition of FAK may be a promi

167 emin (NS) is known to be up-regulated during liver regeneration, and loss of NS is associated with in

168 NAD availability is limiting during liver regeneration, and supplementation with precursors

169 miRNAs are involved in liver regeneration, and their expression is dysregulated

170 in response to hepatic insufficiency promote liver regeneration, and they define specific pro- and an

171 well known, and the mechanisms that regulate liver regeneration are extensively studied.

172 ugh which these two molecules might regulate liver regeneration are not known.

173 tors derived from platelet alpha-granules on liver regeneration are unclear, because alpha-granules c

174 ombination with PVL seem to mediate enhanced liver regeneration, associated with ALPPS.

175 cells and the hepatocytes in the process of liver regeneration by activating the PDK4-mediated metab

176 sp8 comprises a nonapoptotic function during liver regeneration by balancing RIP1, NF-kappaB, and JNK

177 eltaEC)) from the adult mouse liver impaired liver regeneration by diminishing Id1-mediated productio

178 B1Rs) to promote hepatocyte proliferation in liver regeneration by inducing cell cycle proteins invol

179 t is widely assumed that platelets stimulate liver regeneration by local excretion of mitogens stored

180 es also indicate that HDAC activity promotes liver regeneration by regulating hepatocellular cell cyc

181 ation, and IL-4, which indirectly attenuates liver regeneration by stimulating iNKT cell expansion an

182 ehog pathway controls Yap1 activation during liver regeneration by studying intact mice and cultured

183 d rather than suppressed progenitor-mediated liver regeneration by switching progenitor cell differen

184 g embryogenesis will yield insights into how liver regeneration can be promoted and how functional li

185 tes (Casp8(Deltahepa) ) and determined their liver regeneration capacity by measuring liver mass rest

186 ggers NF-kappaB activation and thus improves liver regeneration, combined loss of Casp8 and NEMO impa

187 S in mice induces an unprecedented degree of liver regeneration, comparable with humans.

188 showed that adult HCs offered more effective liver regeneration compared to other cells in Fah-/- mic

189 In liver regeneration, despite increased signaling, PDGFRal

190 ller T cells and liver injury are central in liver regeneration, elucidating their role is important.

191 pro-inflammatory phase does not resolve and liver regeneration fails, with impaired cell cycle entry

192 tudy examined the effect of TCDD exposure on liver regeneration following 70% partial hepatectomy in

193 F-alpha; TNF) plays a critical role early in liver regeneration following partial hepatectomy (PH).

194 were matched for criteria known to influence liver regeneration following PVE: 1) baseline FLR/Total

195 This Review examines liver regeneration from the perspective that BM SPCs tha

196 t of serotonin, as an incomplete mitogen, on liver regeneration has recently been unveiled and is med

197 n HSCs after acute injury and contributes to liver regeneration, however, is not known.

198 its effector proteins in the progression of liver regeneration; however, a detailed mechanistic unde

199 ectomy (PH) and other experimental models of liver regeneration implicate the metabolic response to h

200 f circulating alpha-granule molecules during liver regeneration in 157 patients undergoing partial he

201 n of Fak and investigated the role of Fak in liver regeneration in 2/3 PHx model (removal of 2/3 of t

202 ose of APAP, resulted in early initiation of liver regeneration in a dose-dependent manner, without m

203 the molecular and physiological kinetics of liver regeneration in Adn(-/-) mice.

204 the molecular and physiological kinetics of liver regeneration in Adn-/- mice.

205 po/Yes-associated protein 1 (Yap1), regulate liver regeneration in adulthood.

206 disease, the molecular mechanisms regulating liver regeneration in ALF patients remain largely unknow

207 l framework which described post-hepatectomy liver regeneration in each patient by incorporating quan

208 Transplanted HSCs contributed to liver regeneration in host animals by forming mesenchyma

209 rcadian rhythms, and lipid metabolism during liver regeneration in mice.

210 errupting the hypoglycemic response to PH on liver regeneration in mice.

211 ssure by terlipressin improves postoperative liver regeneration in normal and steatotic livers after

212 AK may be a promising strategy to accelerate liver regeneration in recipients after liver transplanta

213 Consequently, NorUDCA restored liver regeneration in SIRT mice, which showed increased

214 The inhibition of liver regeneration in the APAP600 group was associated w

215 FXR agonists were found to promote liver regeneration in the murine model of APAP induced l

216 cle actin and Ki-67 to establish the role of liver regeneration in the tumorigenic effect of RF ablat

217 We show that liver regeneration in this microenvironment leads to a s

218 contribution of various cell populations to liver regeneration in vivo following several ADC-inducin

219 s issue, we established a zebrafish model of liver regeneration in which the extent of hepatocyte abl

220 eased immediately after PH (priming phase of liver regeneration) in control mice, but this effect was

221 regulation of miRNA target genes that impair liver regeneration, including heme oxygenase-1, programm

222 Liver regeneration induced by RF ablation facilitates c-

223 Conclusion Liver regeneration induced by RF ablation facilitates c-

224 d that increased p21(Cip1) expression during liver regeneration involved an AhR-dependent mechanism.

225 Liver regeneration is a spontaneous process that occurs

226 Liver regeneration is a well-orchestrated process in the

227 Previous studies show that stimulating liver regeneration is critical for survival after APAP o

228 progenitor cells (SHPCs), and hepatocytes in liver regeneration is debated.

229 ce confirmed that TCDD-induced inhibition of liver regeneration is entirely dependent on p21(Cip1) ex

230 Understanding the molecular mechanisms of liver regeneration is essential to improve the survival

231 A challenge for advancing approaches to liver regeneration is loss of functional differentiation

232 Liver regeneration is of crucial importance for patients

233 Liver regeneration is of major clinical importance in th

234 Moreover, liver regeneration is significantly increased by the sca

235 Liver regeneration is stimulated by blood platelets, but

236 ccelerating tissue growth in vivo, including liver regeneration, kidney compensatory growth, lung com

237 ivation of Wnt/beta-catenin signaling during liver regeneration (LR) after partial hepatectomy (PH) i

238 ericentral gene expression and in initiating liver regeneration (LR) after partial hepatectomy (PH),

239 ever, the consequences of Nrf2 activation on liver regeneration (LR) have not been determined.

240 Liver regeneration (LR) involves a complex interplay of

241 The most studied form of liver regeneration (LR) is that occurring after loss of

242 types of liver problems, including impaired liver regeneration (LR), but the mechanism for this is u

243 ty to ischemia reperfusion (I/R) and impedes liver regeneration (LR).

244 ms whereby cell-matrix interactions regulate liver regeneration may allow novel strategies to enhance

245 Our data indicate that human liver regeneration may be orchestrated by distinct miRNA

246 ranscriptional cofactors Ski and SnoN during liver regeneration may favor hepatocyte proliferation by

247 knowledge of mechanisms of platelet-mediated liver regeneration may lead to new therapeutic strategie

248 partial hepatectomy as a surgically induced liver regeneration model we show that adeno-associated v

249 rines replace cysteines, promotes muscle and liver regeneration more efficiently than the wild-type p

250 Liver regeneration occurs in a hypoxic environment.

251 Liver regeneration occurs in a hypoxic environment.

252 Liver regeneration offers a distinctive opportunity to s

253 dy identifies an unanticipated dependence of liver regeneration on MICU1 and highlights the importanc

254 not clear whether these cells contribute to liver regeneration or serve as a progenitor cell populat

255 Liver regeneration peaked at 24 h ([(3)H]-thymidine inco

256 Mobilized Cd39 HSCs boost liver regeneration, potentially limiting interleukin 1be

257 ET knockout + EGFR-inhibited mice) abolishes liver regeneration, prevents restoration of liver mass,

258 n of interleukin-6 (IL6), which is a crucial liver regeneration priming cytokine.

259 te that radiofrequency (RF) ablation-induced liver regeneration promotes "off-target" tumorigenesis i

260 The regulation of specific liver regeneration-promoting signals, including hepatic

261 ted tomography of 123 patients, we estimated liver regeneration rates.

262 hich genes are most important in controlling liver regeneration remains unanswered.

263 However, the function of iNKT cells in liver regeneration remains unclear.

264 The role of FAK in liver regeneration remains unknown.

265 Liver regeneration requires functional liver macrophages

266 Adult liver regeneration requires induction and suppression of

267 t liver injury but substantial inhibition of liver regeneration, resulting in sustained injury and de

268 of the immune system, which are required for liver regeneration, survival, and hepatocarcinogenesis.

269 in this setting, with the prospect of native liver regeneration sustaining long-term survival.

270 During liver regeneration, the concentration of nicotinamide ad

271 hances hepatocyte proliferation and promotes liver regeneration, thereby preventing liver failure.

272 omplement system during the priming phase of liver regeneration through a systems level analysis usin

273 ealed that Adn fine-tunes the progression of liver regeneration through dynamically modulating molecu

274 ealed that Adn fine-tunes the progression of liver regeneration through dynamically modulating molecu

275 underlying adiponectin's (Adn) regulation of liver regeneration through modulation of these mediators

276 underlying Adiponectin's (Adn) regulation of liver regeneration through modulation of these mediators

277 Platelets promote liver regeneration through site-specific serotonin relea

278 nsdifferentiation into cholangiocytes during liver regeneration to restore biliary epithelium integri

279 Accordingly, IL-22 was shown to promote liver regeneration upon acute liver damage.

280 Here we study the role of integrins in mouse liver regeneration using Cre/loxP-mediated gene deletion

281 ion factor X-box binding protein 1 (XBP1) in liver regeneration using genome-wide chromatin immunopre

282 istone deacetylase (Zn-HDAC) activity during liver regeneration using the mouse partial hepatectomy (

283 fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 an

284 Liver regeneration was assessed by BrdU incorporation an

285 The contribution of Hnf1beta(+) cells to liver regeneration was dependent on the liver injury mod

286 Liver regeneration was evaluated by [(3)H]-thymidine inc

287 Liver regeneration was evaluated by Ki67 labeling.

288 Liver regeneration was greatly attenuated when blockade

289 Acceleration of liver regeneration was not secondary to alteration of AP

290 ctivated only in APAP300-treated mice, where liver regeneration was stimulated.

291 hepatitis (NASH) is associated with impaired liver regeneration, we investigated the effects of G49,

292 mal models only partially recapitulate human liver regeneration, we investigated the molecular mechan

293 ether NAD availability restricts the rate of liver regeneration, we supplied nicotinamide riboside (N

294 Benefits in terms of liver regeneration were also found in mice fed HFD and t

295 5-HT7 receptor blockade had no effect on liver regeneration when applied 2 h prior to partial hep

296 Mechanisms that terminate liver regeneration when the liver reaches the original s

297 ral killer T cells play an important role in liver regeneration, which is associated with cyclin B1 a

298 Platelets support liver regeneration, which is required after partial hepa

299 iption factor Foxa3 was a strong promoter of liver regeneration, while tumor necrosis factor receptor

300 tion, the authors demonstrated that blocking liver regeneration with a c-met inhibitor might attenuat