ライフサイエンスコーパス: fibrogenic

1 ogenic potential, c-Kit(+)/PW1(+) cells were fibrogenic.

2 cocktail, dasatinib plus quercetin (DQ), is fibrogenic.

3 f 2 major injury responses: inflammatory and fibrogenic.

4 liver fibrosis and are able to modulate the fibrogenic actions of nonparenchymal liver cells.

5 alcohol-fed rats, were resistant to the anti-fibrogenic actions of ONOO- due to higher levels of GSH,

6 en stabilization in liver fibrosis, promotes fibrogenic activation of attenuated hepatic stellate cel

7 between HCV-infected hepatocytes and HSC in fibrogenic activation.

8 ossesses both important immunomodulatory and fibrogenic activities, and should be considered a key fo

9 bit anti-inflammatory, anti-cancer, and anti-fibrogenic activities, very little is known about its me

10 n the absence of PH, associated with reduced fibrogenic activity (e.g., expression of alpha smooth mu

11 , these observations indicate that increased fibrogenic activity because of dysregulated RhoA GTPase

12 of Sirtuin 1 (Sirt1)/Timp3 pathways mediate fibrogenic activity in NASH.

13 t the link between AGEs and inflammatory and fibrogenic activity in nonalcoholic steatohepatitis (NAS

14 KLF6 reduces fibrogenic activity of HSCs by way of two distinct mecha

15 The fibrogenic activity of NOX2 was assessed by collagen rep

16 y overexpressing HAI-1 or HAI-2 enhanced the fibrogenic activity of portal fibroblasts and stellate c

17 miR-200 family members can reverse the fibrogenic activity of pulmonary fibroblasts from mice w

18 eas knocking down miR-21 attenuated, the pro-fibrogenic activity of TGF-beta1 in fibroblasts.

19 The enhanced fibrogenic activity of the DDX5 risk variant is linked t

20 In conclusion, AR induces hHSC fibrogenic activity via multiple mitogenic signaling pat

21 companied by restored MV density, attenuated fibrogenic activity, and improvements in RBF and GFR gre

22 of renal angiogenic signaling and attenuated fibrogenic activity, which ameliorates MV rarefaction an

23 and invasion of HSCs, contributing to their fibrogenic activity.

24 In response to fibrogenic agonists, such as angiotensin II (Ang II), th

25 induced in fibrotic conditions and modulate fibrogenic and angiogenic responses by regulating growth

26 left ventricular hypertrophy, plays an anti-fibrogenic and anti-hypertrophic role by blocking, among

27 Fibrogenic and contractile activities of lung fibroblast

28 xpression of SEMA7A in HSCs showed increased fibrogenic and inflammation markers expression.

29 t manner, leading to increased expression of fibrogenic and inflammation markers.

30 d oxidative stress, as well as inflammatory, fibrogenic and liver progenitor cell responses, were ass

31 Specifically, potent fibrogenic and prohypertrophic effects, as well as oxida

32 s pancreatic stellate cells (PSCs) to become fibrogenic and secrete chemokines that promote epithelia

33 ngs indicate that IPF MPCs are intrinsically fibrogenic and that S100A4 confers MPCs with fibrogenici

34 CB(1) receptors on hepatic stellate cells is fibrogenic, and CB(1) blockade slows the progression of

35 hotic septa harbor vessels and inflammatory, fibrogenic, and ductular epithelial cells, collectively

36 dase is a crucial mediator of proliferative, fibrogenic, and inflammatory actions of leptin.

37 effects and local expression of angiogenic, fibrogenic, and vasoactive factors.

38 The PAI-1-miR-21 fibrogenic axis also appeared dysregulated in muscle of

39 onal medicine aimed at in vivo modulation of fibrogenic behavior.

40 cular targets of miRNAs that are linked to a fibrogenic cardiac phenotype.

41 a effect on stellate cell activation and the fibrogenic cascade appears to be adiponectin-dependent;

42 l transdifferentiation is a key event in the fibrogenic cascade.

43 EMT activity outstrips MET, repair is mainly fibrogenic, causing liver fibrosis.

44 of activated hepatic stellate cells, the key fibrogenic cell in the liver.

45 ated hepatic stellate cells (HSCs), the main fibrogenic cell type in the liver, undergo apoptosis aft

46 hepatic stellate cells (HSCs), the principle fibrogenic cell type in the liver.

47 ) on hepatic stellate cells (HSCs), the main fibrogenic cell type in the liver.

48 ells (HSCs) have been identified as the main fibrogenic cell type in the liver.

49 show that muscle stem cells communicate with fibrogenic cells by exosomal trafficking of microRNA-206

50 Autophagy was blocked in fibrogenic cells from liver and other tissues using smal

51 xpression also occurred during activation of fibrogenic cells from the adult liver when the transcrip

52 fibrosis remains unclear partly because the fibrogenic cells have not been identified with certainty

53 elective reduction of autophagic activity in fibrogenic cells in liver and other tissues might be use

54 The origin of fibrogenic cells in liver fibrosis remains controversial

55 e cells into proliferative, contractile, and fibrogenic cells in liver injury remains a dominant them

56 we show that MPCs interact with interstitial fibrogenic cells to ensure proper ECM deposition and opt

57 aster regulator of collagen biosynthesis, in fibrogenic cells to prevent excessive ECM deposition.

58 ssue, we demonstrate for the first time that fibrogenic cells within EFE tissue originate from endoca

59 argely of collagens secreted by interstitial fibrogenic cells, which influence satellite cell activit

60 for resolving LF by directly targeting these fibrogenic cells.

61 ivation and extended these findings to other fibrogenic cells.

62 Here, we investigated the role of CTGF in fibrogenic cells.

63 ic chemokine CCL3 and an increase in GFAP(+) fibrogenic cells.

64 uence PF by enhancing fibrogenic factors and fibrogenic cells.

65 effects on the epithelial, inflammatory, and fibrogenic cellular subsets in pancreatic carcinoma and

66 n that a subset of rat lung fibroblasts with fibrogenic characteristics [Thy-1 (-) fibroblasts] respo

67 gic disruptions of MeCP2 or EZH2 reduced the fibrogenic characteristics of myofibroblasts and attenua

68 ules that include a host of inflammatory and fibrogenic, chemokines, cytokines and growth factors.

69 ro-inflammatory (IL-6, iNOS, ICAM-1) and pro-fibrogenic (Col1, alpha-SMA, TIMP-1) genes.

70 an epigenetic suppressive adaptation of the fibrogenic component of wound healing to the male F1 and

71 own of integrin alpha(5) and RhoA attenuated fibrogenic, contractile, and migratory activities of IPF

72 n normal lung fibroblasts and diminishes the fibrogenic, contractile, and migratory activities of IPF

73 Fibrogenic, contractile, and migratory activities of lun

74 termine the role of miR-31 in regulating the fibrogenic, contractile, and migratory activities of lun

75 The pro-fibrogenic cytokine connective tissue growth factor (CTG

76 Interleukin (IL)-17 is a proinflammatory and fibrogenic cytokine mainly produced by T-helper (Th)17 l

77 vation of HSCs and their response to the pro-fibrogenic cytokine TGF-beta was evaluated by gene expre

78 Connective tissue growth factor (CTGF) is a fibrogenic cytokine that is up-regulated by TGF-beta and

79 sforming growth factor (TGF)-beta1, a potent fibrogenic cytokine that is up-regulated in the diseased

80 by subarachnoid fibrosis in which the potent fibrogenic cytokine transforming growth factor-beta has

81 A potent fibrogenic cytokine, transforming growth factor-beta (TG

82 cause IL-13 is a pivotal proinflammatory and fibrogenic cytokine, we examined whether a recombinant i

83 xpression of transforming growth factor-1, a fibrogenic cytokine.

84 fibrogenesis predominantly by producing key fibrogenic cytokines and by promoting cell-to-cell commu

85 tissue inhibitors of metalloproteinases, and fibrogenic cytokines but increased matrix metalloprotein

86 Stimulation of the vagus nerve increases fibrogenic cytokines in humans, therefore, activation of

87 ced HSC activation and their response to pro-fibrogenic cytokines like TGF-beta.

88 e stress, and production of inflammatory and fibrogenic cytokines were measured.

89 xidative stress, apoptosis and production of fibrogenic cytokines.

90 (miR-21) contributes to the pathogenesis of fibrogenic diseases in multiple organs, including the ki

91 eneficial for treating hyperproliferative or fibrogenic diseases of the skin.

92 ystemic hypertension, cancer, vasospasm, and fibrogenic diseases.

93 g growth factor (TGF)-b pathway, a canonical fibrogenic driver, suggesting that XBP1 activates a spec

94 research on whether TGF-beta has a stronger fibrogenic effect in the setting of inflammation is warr

95 DA-deficient mice, we herein report a direct fibrogenic effect of adenosine on the skin, in which inc

96 Mevalonate reversed the anti-fibrogenic effect of CSA13.

97 esenchymal proteins that initiate a cycle of fibrogenic effector cell activation, leading to progress

98 gnaling and whether this is required for the fibrogenic effects of leptin.

99 explores the mechanisms responsible for the fibrogenic effects of Smad3 by dissecting its role in mo

100 including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta.

101 L1), we hypothesize that CSA13 mediates anti-fibrogenic effects via FPRL1.

102 ently develops in a pro-inflammatory and pro-fibrogenic environment with hepatic stellate cells (HSCs

103 and increased risk for adverse vascular and fibrogenic events post-MI.

104 levels in HCV treatment outcomes and in the fibrogenic evolution of HCV-related liver disease.

105 STAT-4-T-allele is identified as fibrogenic factor and seems to have a negative impact on

106 aken together, we identify RGC-32 as a novel fibrogenic factor contributing to the pathogenesis of re

107 ctive tissue growth factor (CTGF) is a major fibrogenic factor.

108 he vagus nerve may influence PF by enhancing fibrogenic factors and fibrogenic cells.

109 n, blocked the induction of ECM proteins and fibrogenic factors and improved respiratory compliance i

110 ession levels of collagen, vimentin, and the fibrogenic factors transforming growth factor beta1 and

111 the notion that both genetic and nongenetic fibrogenic factors, particularly TGF-beta1 and oxidative

112 blast accumulation, and expression levels of fibrogenic factors.

113 t accumulation, and expression levels of the fibrogenic factors.

114 ith increased expression of ECM proteins and fibrogenic factors.

115 mia inhibitory factor (LIF), and IL-11, have fibrogenic features.

116 To better understand the susceptibility of fibrogenic fibroblasts to the stimulation of TGF-beta ac

117 es that can induce osteogenic (biglycan) and fibrogenic (fibromodulin, decorin) phenotypes, and PDL-s

118 E2F1 is a fibrogenic gene and could serve as a potential new diagn

119 Increased fibrogenic gene expression in DDX5 SNP-expressing cells

120 miR-199a-5p accounts, in part, for low-level fibrogenic gene expression in quiescent HSCs and causes

121 id increase in proinflammatory cytokines and fibrogenic gene expression was also observed.

122 epletion of ASH1 caused broad suppression of fibrogenic gene expression.

123 Pro-fibrogenic gene expressions (COL1, TIMP-1, TGF-beta1, al

124 induced alpha-SMA protein expression and pro-fibrogenic gene expressions in HSC-T6 were suppressed in

125 malized but the lung fibrotic abnormalities, fibrogenic gene induction and pulmonary elasticity were

126 ), whose depletion upon activation induces a fibrogenic gene program.

127 promote fibrogenesis through coregulation of fibrogenic gene targets.

128 ized that the activity of DDX5 in regulating fibrogenic gene transcription in hepatic stellate cells

129 6 in liver injury may allow de-repression of fibrogenic genes and decreased stellate cell clearance b

130 direct transcriptional repression of target fibrogenic genes and increased apoptosis of activated HS

131 ) HSCs were unable to increase expression of fibrogenic genes IL-1beta and tissue inhibitor of metall

132 Autophagy also regulated expression of fibrogenic genes in embryonic, lung, and renal fibroblas

133 ese data suggest that DDX5 is a repressor of fibrogenic genes in HSCs through interaction with transc

134 mRNA expression of pro-inflammatory and pro-fibrogenic genes in livers of CDAA rats.

135 s, but did not demonstrate the inhibition of fibrogenic genes observed in pn.

136 regression of liver fibrosis, down-regulate fibrogenic genes, and acquire a phenotype similar to, bu

137 H incidence and inductions of progenitor and fibrogenic genes, but rather enhances the Il-17a inducti

138 iated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle act

139 hepatic fibrosis, with reduced expression of fibrogenic genes, compared to WT mice.

140 drial DNA deletions, and renal expression of fibrogenic genes, including transforming growth factor b

141 lipid morphology and increased expression of fibrogenic genes, suggesting they are primed for activat

142 minished fibrosis with reduced expression of fibrogenic genes.

143 on of stellate cells and expression of human fibrogenic genes.

144 ochondrial DNA damage and over expression of fibrogenic genes.

145 pression and enhanced promoter activities of fibrogenic genes.

146 play an important role in the production of fibrogenic growth factors and development of fibrosis.

147 d c-Myc), leading to increased expression of fibrogenic growth factors, activation of cell cycle sign

148 e resulting offspring better adapt to future fibrogenic hepatic insults.

149 Effects of LPS on fibrogenic hepatic stellate cells (HSCs) from WT and TLR

150 Here we report that fibrogenic hepatic stellate cells (HSCs) in the liver ar

151 Thus, XBP1-mediated UPR contributes to fibrogenic HSC activation and is functionally linked to

152 GIV is expressed in the liver after fibrogenic injury and is required for HSC activation.

153 inhibited PMC migration after intratracheal fibrogenic injury.

154 g no evidence for MET in HSCs in response to fibrogenic liver injury.

155 Our previous study showed that isolated fibrogenic lung fibroblasts have high endogenous levels

156 tion, and caused substantial increase in the fibrogenic marker miR-21 expression, indicating the high

157 scle actin staining and expression levels of fibrogenic markers (eg, transforming growth factor-beta1

158 ture, paralleling the enhanced expression of fibrogenic markers alpha-smooth muscle actin (alpha-SMA)

159 AR also induced marked upregulation of hHSC fibrogenic markers and reduced hHSC death.

160 ion of Rev-erbalpha, decreased expression of fibrogenic markers and the activated phenotype in HSCs,

161 ced the leptin-mediated up-regulation of the fibrogenic markers collagen alpha1(I) and alpha-smooth m

162 uced HSC proliferation and expression of pro-fibrogenic markers of mouse and human HSCs.

163 dystrophy (DMD) patients, yet the implicated fibrogenic mechanisms remain poorly understood.

164 This reflects its capacity to stimulate fibrogenic mediators and induce the expression of other

165 repressed the expression of inflammatory and fibrogenic mediators in primary Kupffer cells.

166 as betaTRCP-dependent degradation of the pro-fibrogenic mediators Sp1, TAZ and beta-catenin.

167 igate the expression of the inflammatory and fibrogenic mediators which may be involved.

168 viously discovered that the IPF lung harbors fibrogenic mesenchymal progenitor cells (MPCs) that serv

169 These fibrogenic mesenchymal progenitors and their progeny rep

170 ignificantly increased fibrosis and enhanced fibrogenic messenger RNA (mRNA) and protein expression.

171 nAChRalpha1) was investigated as a potential fibrogenic molecule in the kidney, given reports that it

172 l cell coverage fostered the accumulation of fibrogenic molecules and the attraction of fibroblasts t

173 We have therefore been able to convert pro-fibrogenic myofibroblasts in the liver into hepatocyte-l

174 rentiate in the setting of chronic injury to fibrogenic myofibroblasts, playing an important role in

175 ic stellate cells or portal fibroblasts into fibrogenic myofibroblasts.

176 hese findings indicate that T-cell-regulated fibrogenic pathways are highly mechanoresponsive and sug

177 Over time, inflammation and fibrogenic pathways become dominant while in advanced di

178 essential for activation of inflammatory and fibrogenic pathways in the healing infarct, playing an i

179 Fibrogenic pathways in the liver are principally regulat

180 at altered chitin clearance could exacerbate fibrogenic pathways in the setting of lung diseases char

181 ss-talk regulating cell fate-determining and fibrogenic pathways.

182 of genes involved in immune responses and in fibrogenic pathways.

183 cardiac fibrosis via regulation of multiple fibrogenic pathways.

184 drive fibrogenesis by modulating the HSC pro-fibrogenic phenotype and Collagen-I expression.

185 e pathogenesis of fibrosis by regulating the fibrogenic phenotype of hepatic stellate cells (HSCs).

186 he induced cellular responses that drive the fibrogenic phenotype remain to be elucidated.

187 The key mediators of the fibroblast fibrogenic phenotype were characterized using a novel as

188 om mice infected with B. abortus displayed a fibrogenic phenotype with patches of collagen deposition

189 1 expression appears to be necessary for the fibrogenic phenotype, an idea supported by evidence that

190 ells could be turned into an inflammatory or fibrogenic phenotype.

191 y (M1 cells) as well as antiinflammatory and fibrogenic phenotypes (M2 cells); they affect transplant

192 , including: (1) identification of different fibrogenic populations apart from resident stellate cell

193 el alternative splice form that modifies the fibrogenic potential of HSCs.

194 arker miR-21 expression, indicating the high fibrogenic potential of this specific carbon nanotube ty

195 indicating increased activation of HSCs and fibrogenic potential.

196 iscusses the role of nicotine in the general fibrogenic process that governs fibrosis and fibrosis-re

197 We describe a novel role of leptin in the fibrogenic process, the induction of phagocytosis of apo

198 oblasts to myofibroblasts, a hallmark of the fibrogenic process, using pulmonary fibroblasts isolated

199 ulates HSC activation and inhibits the liver fibrogenic process.

200 l-characterized cholestatic inflammatory and fibrogenic process; however, the mechanisms and potentia

201 rgan-resident, mesenchymal precursors in the fibrogenic processes in human adult lungs.

202 transmembrane protein Cx43 has key roles in fibrogenic processes including inflammatory signaling an

203 ay simultaneously block the inflammatory and fibrogenic processes of PF.

204 xpression is shown to impair TGF-beta-driven fibrogenic processes, including cell proliferation and p

205 d with various immune, hepatoprotective, and fibrogenic processes.

206 protects against organ fibrosis by removing fibrogenic products of lipid peroxidation.

207 Targeting the fibrogenic progenitor response represents a promising st

208 A miR-21 as a long-term memory keeper of the fibrogenic program in MSCs.

209 perglycemia-induced epigenetic activation of fibrogenic program in the kidney.

210 a from Lxralphabeta(-/-) cells increases the fibrogenic program of wild-type cells.

211 HSC FA utilization and in turn regulates the fibrogenic program.

212 ung fibroblasts differentially contribute to fibrogenic progression.

213 Within days a fibrogenic, proliferative mechanism causes anatomic clos

214 nd in inflammatory zone 1 (FIZZ1) has direct fibrogenic properties because of its ability to induce m

215 n-associated vascular remodeling, as well as fibrogenic properties during pulmonary fibrosis.

216 tenuated hypoxia-induced upregulation of the fibrogenic protein connective tissue growth factor and c

217 nt autocrine signalling that is required for fibrogenic protein synthesis.

218 vels and diminished liver expression of anti-fibrogenic receptor CB2.

219 e signaling between an immune cytokine and a fibrogenic receptor.

220 RelA-P-Ser536 may be a core fibrogenic regulator of fibroblast phenotype.

221 effects of increased Hh signaling on EMT and fibrogenic repair during diet-induced NAFLD were also co

222 This study evaluated the hypothesis that fibrogenic repair in nonalcoholic fatty liver disease (N

223 The mechanism that triggers the fibrogenic response after injury is not well understood.

224 iferation using anti-TWEAK antibody prevents fibrogenic response and augments fibrotic liver regenera

225 p-regulation of Rev-erbalpha is an intrinsic fibrogenic response characterized by cytoplasmic accumul

226 inhibited and is tightly associated with the fibrogenic response during severe liver damage.

227 y reported the ability of KC to induce a pro-fibrogenic response in HSC via reactive oxygen species (

228 HSC(ethanol) proliferation; however, the pro-fibrogenic response in HSC(ethanol) was suppressed becau

229 with SIN-1 or ONOO- reduced the TGFbeta pro-fibrogenic response in HSC.

230 ns, which could help explain the exaggerated fibrogenic response in IPF.

231 deposition; furthermore, AA restored the pro-fibrogenic response in the HSC(ethanol) co-cultures by c

232 fat overload which promotes inflammatory and fibrogenic response similar to those observed in patient

233 Therefore, the senescence program limits the fibrogenic response to acute tissue damage.

234 did not affect immune cell migration or the fibrogenic response to chronic liver injury.

235 ivation as well as signaling cascades in the fibrogenic response to injury.

236 lagen are targets for regulating the initial fibrogenic response to liver damage.

237 Systemic VEGF overexpression led to a fibrogenic response within the liver and was associated

238 genitor (oval) cell compartment and a severe fibrogenic response.

239 ssion of key matrix genes, consistent with a fibrogenic response.

240 se alcohol-induced liver injury and an early fibrogenic response.

241 ed the protective role of ONOO- on the early fibrogenic response.

242 ivation and modulate the stellate cell (HSC) fibrogenic response.

243 o the understanding of the TGF-beta-mediated fibrogenic response.

244 K) activity and disrupts key features of the fibrogenic response.

245 operates downstream of FAK/Src in mediating fibrogenic responses and that targeting of TAK1 may be a

246 ole of pancreatic acinar cells in initiating fibrogenic responses during the early stages of alcoholi

247 ng HSCs, but not on the BM, was required for fibrogenic responses in chronic fibrosis models.

248 (TAK1) acts downstream of FAK/Src to mediate fibrogenic responses in fibroblasts.

249 yte-derived OPN and recombinant OPN promoted fibrogenic responses in HSCs (P < 0.05); neutralizing OP

250 IL-1beta induced fibrogenic responses in HSCs, including secretion of tis

251 Chemical analogs of 4MU also inhibited fibrogenic responses in proportion to their inhibition o

252 wever, the role of inflammatory mediators in fibrogenic responses of the liver is only poorly underst

253 signaling in liver fibrosis, we compared the fibrogenic responses of wild-type (WT) and tpl2(-/-) mic

254 o RNAi-mediated silencing of CCN1 attenuates fibrogenic responses to bleomycin-induced lung injury.

255 signaling in fibroblasts and contributes to fibrogenic responses to lung injury.

256 planted mesenchymal cells, Wnt-3a stimulated fibrogenic responses while suppressing adipogenesis.

257 SCs were isolated to assess inflammatory and fibrogenic responses, respectively.

258 s off a complex sequence of inflammatory and fibrogenic responses.

259 and immunoblotting were performed to assess fibrogenic responses.

260 oduce factors that modulate inflammatory and fibrogenic responses.

261 nterstitial lung fibroblasts is critical for fibrogenic responses.

262 To screen the fibrogenic risk factor of specific types of MWCNT, we de

263 These data confirm a fibrogenic role for adenosine in the skin and reveal A(2

264 Here, we demonstrate key determinants of the fibrogenic set point of cardiac fibroblasts (CFs) by foc

265 athway and downstream MMP-12 in a variety of fibrogenic settings.

266 Given the importance of TGF-beta1 as a fibrogenic signal, a microsystem with integrated biosens

267 ge CD36 is a critical regulator of oxidative fibrogenic signaling and that CD36-mediated phagocytosis

268 The fibrogenic signaling events downstream of TLRs on Kupffe

269 tor (PDGF), place NADPH in the center of the fibrogenic signaling response in HSCs and demonstrate it

270 melanocyte growth stasis, nevus biology, and fibrogenic signaling was further validated in vivo by th

271 lizes transactivation mechanisms to initiate fibrogenic signaling.

272 F), which serves as a central hub within the fibrogenic signalling network initiated by diverse class

273 chanism that regulates cardiomyocyte-derived fibrogenic signals and cardiac transcriptional pathways

274 hepatocytes produce hepato-inductive and pro-fibrogenic signals at the levels sufficient to shape the

275 Fibrogenic signals drive transcription of procollagen I,

276 ance activation of HSCs and induction of the fibrogenic signals in these cells.

277 Hypothesizing that early fibrogenic signals may originate in cells susceptible to

278 nsumption sensitizes HSC to up-regulate anti-fibrogenic signals, their effects are blunted by a secon

279 iologic Epo-producing state and a pathologic fibrogenic state in response to microenvironmental signa

280 responsiveness of reverted HSCs to recurring fibrogenic stimulation.

281 eactivate into myofibroblasts in response to fibrogenic stimuli and strongly contribute to liver fibr

282 fully characterized, we aimed to analyze the fibrogenic stimuli in a new in vitro model of NASH.

283 ular mechanism linking hypoxia signaling and fibrogenic stimuli in the lungs.

284 egenerate hepatocytes in various contexts of fibrogenic stimuli remain elusive.

285 ions direct the cellular response of HPCs to fibrogenic stimuli, but also identify novel potential th

286 llular matrix organization and is induced by fibrogenic stimuli.

287 ate, with higher levels of responsiveness to fibrogenic stimuli.

288 Following a fibrogenic stimulus the cell changes from a quiescent vi

289 kin, predominantly in the adipogenic but not fibrogenic subsets.

290 ibroblasts, and suppressed expression of the fibrogenic TGF-beta1, CTGF, fibronectin, and types I and

291 SH, a ONOO- scavenger, overproduction of pro-fibrogenic TGFbeta, and reactive oxygen species.

292 th factor (TGF)-beta activation, whereas non-fibrogenic Thy-1-expressing [Thy-1 (+)] fibroblasts do n

293 al cells toward myofibroblasts by inducing a fibrogenic transcriptional program while suppressing adi

294 Some fibrogenic transcriptional responses to transforming gro

295 TNF-alpha production as well as induction of fibrogenic transcripts.

296 th a significant increase in GSSG and in pro-fibrogenic transforming growth factor beta (TGF-beta).

297 or could regulate the bioavailability of the fibrogenic transforming growth factor beta in response t

298 lpha responded to both adipogenic ligand and fibrogenic transforming growth factor beta treatment.

299 ional repressor activity was not affected by fibrogenic treatments.

300 The subsequent fibrogenic/wound-healing response to both chronic carbon