ライフサイエンスコーパス: liver regeneration

1 adult hepatocytes did not noticeably impair liver regeneration.

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

3 stem cells and their derived hepatocytes for liver regeneration.

4 fter APAP overdose is associated with timely liver regeneration.

5 gated the potential contribution of AnxA6 in liver regeneration.

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

7 ic properties of hepatocytes with respect to liver regeneration.

8 Oxygen is a key regulator of liver regeneration.

9 latelets within the liver after induction of liver regeneration.

10 d quantitative insights into the dynamics of liver regeneration.

11 endothelial cell-hepatocyte crosstalk during liver regeneration.

12 ntrol morphogenic signaling during effective liver regeneration.

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

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

15 ile ducts caused severe defects and delay in liver regeneration.

16 atalytic activity during the early stages of liver regeneration.

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

18 adult liver progenitors that participate in liver regeneration.

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

20 Tgf-beta upregulation during early stage of liver regeneration.

21 nd that specific deletion of Fak accelerates liver regeneration.

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

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

24 The rat is an important model for liver regeneration.

25 chanisms that are involved in termination of liver regeneration.

26 ap, increased Hippo activity, and suppressed liver regeneration.

27 echanism may contribute to platelet-mediated liver regeneration.

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

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

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

31 also accumulate in the liver during impaired liver regeneration.

32 lesterol uptake into hepatocytes and affects liver regeneration.

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

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

35 vation of proregenerative genes and enhanced liver regeneration.

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

37 tion and liver marker gene expression during liver regeneration.

38 as regulated during and essential for normal liver regeneration.

39 some recover spontaneously and show complete liver regeneration.

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

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

42 ns for the understanding and manipulation of liver regeneration.

43 differentiate to hepatocytes contributing to liver regeneration.

44 production by iNKT cells, markedly inhibited liver regeneration.

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

46 inhibiting bacterial infection and promoting liver regeneration.

47 developed extensive liver injury and robust liver regeneration.

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

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

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

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

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

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

54 totally reversed the observed attenuation of liver regeneration.

55 ost-injury alterations of gene expression in liver regeneration.

56 ing promotes recovery from injury and drives liver regeneration.

57 al regulator of hepatocyte proliferation and liver regeneration.

58 tor ABT-737 blunts p21 expression, enhancing liver regeneration.

59 0%, whereas systemic MMP inhibition impaired liver regeneration.

60 This ameliorates injury and accelerates liver regeneration.

61 s mimicking the signaling events involved in liver regeneration.

62 get to inhibit liver fibrosis and to promote liver regeneration.

63 utions of injury-induced LPLCs to periportal liver regeneration.

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

65 cial role in the cellular crosstalk of rapid liver regeneration.

66 rograms with potential applications to adult liver regeneration.

67 ated the steatosis that normally accompanies liver regeneration.

68 with anti CD1d antibodies exhibited reduced liver regeneration.

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

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

71 During liver regeneration, a clone of hepatocytes that expresse

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

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

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

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

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

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

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

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

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

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

82 Liver regeneration after APAP-induced liver injury is do

83 te recent efforts to study the mechanisms of liver regeneration after APAP-induced liver injury, more

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

85 We evaluated liver regeneration after carbon tetrachloride toxic live

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

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

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

89 We monitored liver regeneration after hepatocyte ablation and HCC dev

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

91 identity of cellular populations that drive liver regeneration after injury is the subject of intens

92 Liver regeneration after injury requires fine-tune regul

93 ease hepatocyte proliferation and accelerate liver regeneration after injury.

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

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

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

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

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

99 terleukin-6 (IL-6) is critically involved in liver regeneration after partial hepatectomy (PHX).

100 Moreover, liver regeneration after partial hepatectomy also depend

101 EDHB selectively augmented liver regeneration after partial hepatectomy and portal

102 We used liver regeneration after partial hepatectomy as a physio

103 liver-selective MMP-9 inhibition accelerated liver regeneration after partial hepatectomy by 40%, whe

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

105 sed hepatocyte proliferation and accelerated liver regeneration after partial hepatectomy in mice.

106 Platelets play a pivotal role in stimulating liver regeneration after partial hepatectomy in rodents

107 (EGFR), are known to play a critical role in liver regeneration after partial hepatectomy, but their

108 mice have altered cell cycle progression and liver regeneration after partial hepatectomy, suggesting

109 Using a model of liver regeneration after partial hepatectomy, we found t

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

111 FR can also regulate lipid metabolism during liver regeneration after partial hepatectomy.

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

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

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

115 indicating that fibrin(ogen) contributes to liver regeneration after PHx by promoting intrahepatic p

116 erm contribution of IL-6 trans-signaling for liver regeneration after PHX is unknown.

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 ompensates for disabled classic signaling in liver regeneration after PHX.

120 deposition drives platelet accumulation and liver regeneration after PHx.

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

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

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

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

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

126 The augmenter of liver regeneration (ALR) protein is critical for lipid h

127 Levels of augmenter of liver regeneration (ALR), a multifunctional protein, are

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

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

130 Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabolism by modulatin

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

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

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

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

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

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

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

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

139 TCS-mediated liver regeneration and fibrosis preceded HCC development

140 I/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with e

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 Liver regeneration and metabolism are highly interconnec

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

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

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

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

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

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

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

160 We performed partial hepatectomies to test liver regeneration and then RNA-sequencing to identify c

161 This slowed liver regeneration and was associated with reduced expre

162 proliferation during zebrafish development, liver regeneration, and carcinogenesis.

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

164 usoidal endothelial cell integrity, enhanced liver regeneration, and reduced ascites.

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

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

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

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

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

170 rther our understanding of key regulators of liver regeneration as well as patient populations that a

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

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

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

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

175 Rather, YAP/TAZ play an indirect role in liver regeneration by preserving bile duct integrity and

176 hypothesis that fibrin(ogen) contributes to liver regeneration by promoting intrahepatic platelet ac

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

178 tion and has proved difficult to manipulate, liver regeneration can be potentially modulated even in

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

180 ice show a decrease in SIRT1 activity during liver regeneration, coincidentally with DN-DBC1 downregu

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

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

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

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

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

186 stablish a ductular reaction (DR) to support liver regeneration following injury.

187 gnaling, but not classic signaling, controls liver regeneration following PHX.

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

189 and, consequently, alleviating repression of liver regeneration genes, priming them for expression in

190 ce, but the role of fibrin(ogen) deposits in liver regeneration has not been investigated.

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

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

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

194 ls represent an exciting new cell source for liver regeneration; however, culturing large numbers of

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

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

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

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

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

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

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

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

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

204 ments, non-hepatocytes did not contribute to liver regeneration in mice with increased polyploidy.

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

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

207 AnxA6 compromises alanine-dependent GNG and liver regeneration in mice.

208 methylation, as dynamically expressed during liver regeneration in mice.

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

210 nt a promising therapeutic strategy to drive liver regeneration in patients with a broad range of liv

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

212 Liver regeneration in rodents is delayed when platelets

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 APAP hepatotoxicity-induced liver regeneration involves a complex time- and dose-dep

226 Liver regeneration is a spontaneous process that occurs

227 Liver regeneration is a well-orchestrated process in the

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

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 Liver regeneration is impaired in mice with hepatocyte-s

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

233 Liver regeneration is of crucial importance for patients

234 Liver regeneration is stimulated by blood platelets, but

235 odels of periportal liver injury and impairs liver regeneration, leading to organ dysfunction.

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

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

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

239 Liver regeneration (LR) involves a complex interplay of

240 However, the role of HNF4alpha in liver regeneration (LR) is not known.

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 an polyploid cells, both in vitro and during liver regeneration (LR).

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

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

249 Liver regeneration occurs in a hypoxic environment.

250 Liver regeneration offers a distinctive opportunity to s

251 XIN2 and LGR5 after injury and contribute to liver regeneration on demand, without zonal dominance by

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

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

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

255 -art systems biology approaches to models of liver regeneration, pharmacologically and genetically ac

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

257 PHx, indicating that thrombin contributes to liver regeneration primarily by driving intrahepatic fib

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 Augmenter of liver regeneration protein deficiency promotes hepatic s

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

263 sms whereby platelets accumulate and promote liver regeneration remain uncertain.

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

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

266 The role of FAK in liver regeneration remains unknown.

267 Liver regeneration requires functional liver macrophages

268 Adult liver regeneration requires induction and suppression of

269 Liver regeneration requires the organized and sequential

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

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

272 During liver regeneration, the concentration of nicotinamide ad

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

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 compare liver regeneration upon partial hepatectomy in young and

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

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

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

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

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

286 Liver regeneration was evaluated by Ki67 labeling.

287 Liver regeneration was greatly attenuated when blockade

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

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

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

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

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

293 5-HT7 receptor blockade had no effect on liver regeneration when applied 2 h prior to partial hep

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

295 ereby ameliorate liver injury and accelerate liver regeneration, whereas systemic MMP inhibition woul

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

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

298 g APAP overdose, is followed by compensatory liver regeneration, which promotes recovery and is a cru

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