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1  cocktail, dasatinib plus quercetin (DQ), is fibrogenic.
2 tiates from circulating monocytes and is pro-fibrogenic.
3 f 2 major injury responses: inflammatory and fibrogenic.
4 ogenic potential, c-Kit(+)/PW1(+) cells were fibrogenic.
5 roblasts are major targets of TGF-beta, some fibrogenic actions may reflect activation of other cell
6  liver fibrosis and are able to modulate the fibrogenic actions of nonparenchymal liver cells.
7 s) transdifferentiate into proliferative and fibrogenic activated myofibroblastic phenotype (activate
8 attenuate HSC activation, leading to reduced fibrogenic activation in zebrafish, culture-activated HS
9 en stabilization in liver fibrosis, promotes fibrogenic activation of attenuated hepatic stellate cel
10  between HCV-infected hepatocytes and HSC in fibrogenic activation.
11 ossesses both important immunomodulatory and fibrogenic activities, and should be considered a key fo
12 n the absence of PH, associated with reduced fibrogenic activity (e.g., expression of alpha smooth mu
13 with the induction of epithelial plasticity, fibrogenic activity and mechanosensitive Yap/Taz transcr
14 , these observations indicate that increased fibrogenic activity because of dysregulated RhoA GTPase
15  of Sirtuin 1 (Sirt1)/Timp3 pathways mediate fibrogenic activity in NASH.
16 ance and consequent redox, inflammatory, and fibrogenic activity in NASH.
17 t the link between AGEs and inflammatory and fibrogenic activity in nonalcoholic steatohepatitis (NAS
18                                 KLF6 reduces fibrogenic activity of HSCs by way of two distinct mecha
19 y overexpressing HAI-1 or HAI-2 enhanced the fibrogenic activity of portal fibroblasts and stellate c
20       miR-200 family members can reverse the fibrogenic activity of pulmonary fibroblasts from mice w
21               In conclusion, AR induces hHSC fibrogenic activity via multiple mitogenic signaling pat
22 companied by restored MV density, attenuated fibrogenic activity, and improvements in RBF and GFR gre
23 of renal angiogenic signaling and attenuated fibrogenic activity, which ameliorates MV rarefaction an
24  and invasion of HSCs, contributing to their fibrogenic activity.
25                               In response to fibrogenic agonists, such as angiotensin II (Ang II), th
26  induced in fibrotic conditions and modulate fibrogenic and angiogenic responses by regulating growth
27  left ventricular hypertrophy, plays an anti-fibrogenic and anti-hypertrophic role by blocking, among
28                                              Fibrogenic and contractile activities of lung fibroblast
29 nes that act on epithelial cells, as well as fibrogenic and immunosuppressive cytokines that interfer
30 xpression of SEMA7A in HSCs showed increased fibrogenic and inflammation markers expression.
31 t manner, leading to increased expression of fibrogenic and inflammation markers.
32 d oxidative stress, as well as inflammatory, fibrogenic and liver progenitor cell responses, were ass
33                         Specifically, potent fibrogenic and prohypertrophic effects, as well as oxida
34 s pancreatic stellate cells (PSCs) to become fibrogenic and secrete chemokines that promote epithelia
35 ngs indicate that IPF MPCs are intrinsically fibrogenic and that S100A4 confers MPCs with fibrogenici
36 CB(1) receptors on hepatic stellate cells is fibrogenic, and CB(1) blockade slows the progression of
37 hotic septa harbor vessels and inflammatory, fibrogenic, and ductular epithelial cells, collectively
38 ings were associated with necroinflammatory, fibrogenic, and pro-oxidant activity via the NADPH oxida
39 ultiple subtypes of CAFs with diverse roles, fibrogenic, and secretory.
40  effects and local expression of angiogenic, fibrogenic, and vasoactive factors.
41                             The PAI-1-miR-21 fibrogenic axis also appeared dysregulated in muscle of
42 onal medicine aimed at in vivo modulation of fibrogenic behavior.
43  essential regulator of cardiac PW1(+) cells fibrogenic behavior.
44 cular targets of miRNAs that are linked to a fibrogenic cardiac phenotype.
45 a effect on stellate cell activation and the fibrogenic cascade appears to be adiponectin-dependent;
46 l transdifferentiation is a key event in the fibrogenic cascade.
47 irectly activate hepatic stellate cells, the fibrogenic cell in the liver, and drive liver scarring.
48 of activated hepatic stellate cells, the key fibrogenic cell in the liver.
49 ated hepatic stellate cells (HSCs), the main fibrogenic cell type in the liver, undergo apoptosis aft
50 ells (HSCs) have been identified as the main fibrogenic cell type in the liver.
51 fibroblast subpopulation and the predominant fibrogenic cell type.
52 show that muscle stem cells communicate with fibrogenic cells by exosomal trafficking of microRNA-206
53                     Autophagy was blocked in fibrogenic cells from liver and other tissues using smal
54  fibrosis remains unclear partly because the fibrogenic cells have not been identified with certainty
55 elective reduction of autophagic activity in fibrogenic cells in liver and other tissues might be use
56 ealed their specification from adipogenic to fibrogenic cells in the rat model of atrial cardiomyopat
57 we show that MPCs interact with interstitial fibrogenic cells to ensure proper ECM deposition and opt
58 aster regulator of collagen biosynthesis, in fibrogenic cells to prevent excessive ECM deposition.
59 angiotensin II and the relative abundance of fibrogenic cells were sexually dimorphic.
60 ssue, we demonstrate for the first time that fibrogenic cells within EFE tissue originate from endoca
61  are embedded into a dense stroma containing fibrogenic cells, lymphatics and a variety of immune cel
62 argely of collagens secreted by interstitial fibrogenic cells, which influence satellite cell activit
63    Here, we investigated the role of CTGF in fibrogenic cells.
64 hey respond to ischemic damage by generating fibrogenic cells.
65 ic chemokine CCL3 and an increase in GFAP(+) fibrogenic cells.
66 uence PF by enhancing fibrogenic factors and fibrogenic cells.
67 ivation and extended these findings to other fibrogenic cells.
68 nduced a differentiated phenotype in HCC and fibrogenic cells.
69  in human HCC cells and their crosstalk with fibrogenic cells.
70 for resolving LF by directly targeting these fibrogenic cells.
71 effects on the epithelial, inflammatory, and fibrogenic cellular subsets in pancreatic carcinoma and
72                                Each of these fibrogenic changes was restored to control levels by the
73              However, LPS can also attenuate fibrogenic characteristics of aHSCs.
74 ro-inflammatory (IL-6, iNOS, ICAM-1) and pro-fibrogenic (Col1, alpha-SMA, TIMP-1) genes.
75  an epigenetic suppressive adaptation of the fibrogenic component of wound healing to the male F1 and
76 creased capacity to synthesize collagens and fibrogenic components.
77 own of integrin alpha(5) and RhoA attenuated fibrogenic, contractile, and migratory activities of IPF
78 n normal lung fibroblasts and diminishes the fibrogenic, contractile, and migratory activities of IPF
79                                              Fibrogenic, contractile, and migratory activities of lun
80 termine the role of miR-31 in regulating the fibrogenic, contractile, and migratory activities of lun
81                                      The pro-fibrogenic cytokine connective tissue growth factor (CTG
82 h control mice, accompanied by increased pro-fibrogenic cytokine expression but without a significant
83 Interleukin (IL)-17 is a proinflammatory and fibrogenic cytokine mainly produced by T-helper (Th)17 l
84 vation of HSCs and their response to the pro-fibrogenic cytokine TGF-beta was evaluated by gene expre
85  Connective tissue growth factor (CTGF) is a fibrogenic cytokine that is up-regulated by TGF-beta and
86 by subarachnoid fibrosis in which the potent fibrogenic cytokine transforming growth factor-beta has
87                  These lesions overexpress a fibrogenic cytokine, TGFbeta, and an oncogene, ERBB2, ac
88 cause IL-13 is a pivotal proinflammatory and fibrogenic cytokine, we examined whether a recombinant i
89 xpression of transforming growth factor-1, a fibrogenic cytokine.
90  fibrogenesis predominantly by producing key fibrogenic cytokines and by promoting cell-to-cell commu
91 mation of ductular scars by upregulating pro-fibrogenic cytokines and positively regulating collagen-
92 tissue inhibitors of metalloproteinases, and fibrogenic cytokines but increased matrix metalloprotein
93     Stimulation of the vagus nerve increases fibrogenic cytokines in humans, therefore, activation of
94 ced HSC activation and their response to pro-fibrogenic cytokines like TGF-beta.
95 e stress, and production of inflammatory and fibrogenic cytokines were measured.
96 xidative stress, apoptosis and production of fibrogenic cytokines.
97  (miR-21) contributes to the pathogenesis of fibrogenic diseases in multiple organs, including the ki
98 eneficial for treating hyperproliferative or fibrogenic diseases of the skin.
99 ystemic hypertension, cancer, vasospasm, and fibrogenic diseases.
100 g growth factor (TGF)-b pathway, a canonical fibrogenic driver, suggesting that XBP1 activates a spec
101  research on whether TGF-beta has a stronger fibrogenic effect in the setting of inflammation is warr
102                 Mevalonate reversed the anti-fibrogenic effect of CSA13.
103 esenchymal proteins that initiate a cycle of fibrogenic effector cell activation, leading to progress
104 L1), we hypothesize that CSA13 mediates anti-fibrogenic effects via FPRL1.
105 ta) is a potent inducer of developmental and fibrogenic EMTs(4,9,10).
106 r coordinated induction of developmental and fibrogenic EMTs.
107 ently develops in a pro-inflammatory and pro-fibrogenic environment with hepatic stellate cells (HSCs
108  and increased risk for adverse vascular and fibrogenic events post-MI.
109  levels in HCV treatment outcomes and in the fibrogenic evolution of HCV-related liver disease.
110             STAT-4-T-allele is identified as fibrogenic factor and seems to have a negative impact on
111 aken together, we identify RGC-32 as a novel fibrogenic factor contributing to the pathogenesis of re
112                       However, OPN acts as a fibrogenic factor independently of its phosphorylation s
113 he vagus nerve may influence PF by enhancing fibrogenic factors and fibrogenic cells.
114 n, blocked the induction of ECM proteins and fibrogenic factors and improved respiratory compliance i
115  cells in vitro but not any of the other pro-fibrogenic factors assessed.
116    We aimed to analyse the production of pro-fibrogenic factors by airway epithelium in response to A
117 RREB1 directly drive expression of SNAIL and fibrogenic factors stimulating myofibroblasts, promoting
118  the notion that both genetic and nongenetic fibrogenic factors, particularly TGF-beta1 and oxidative
119         We assessed the induction of key pro-fibrogenic factors, TGF-beta1, TGF-beta2, periostin and
120 ith increased expression of ECM proteins and fibrogenic factors.
121  several rate-limiting lipogenic enzymes and fibrogenic factors.
122 mia inhibitory factor (LIF), and IL-11, have fibrogenic features.
123 producing a secretory CAF phenotype with low fibrogenic features; and increased secretion of pro-tumo
124 es that can induce osteogenic (biglycan) and fibrogenic (fibromodulin, decorin) phenotypes, and PDL-s
125 CTA2, ELN, and COL1A1, indicating these were fibrogenic FLC cells.
126 ally dysfunctional due to its acquisition of fibrogenic functions.
127                                    E2F1 is a fibrogenic gene and could serve as a potential new diagn
128 rding the roles of these viral infections on fibrogenic gene expression in LX-2 cells.
129 ral infections on the phenotypic changes and fibrogenic gene expression in LX-2 cells.
130 infection in MLH co-culture had no impact on fibrogenic gene expression in LX-2 cells.
131 miR-199a-5p accounts, in part, for low-level fibrogenic gene expression in quiescent HSCs and causes
132 tivated B cells signaling without increasing fibrogenic gene expression or cell proliferation.
133 id increase in proinflammatory cytokines and fibrogenic gene expression was also observed.
134 ta stimulation of rat or human PCLSs induced fibrogenic gene expression, release of extracellular mat
135 epletion of ASH1 caused broad suppression of fibrogenic gene expression.
136                                          Pro-fibrogenic gene expressions (COL1, TIMP-1, TGF-beta1, al
137 induced alpha-SMA protein expression and pro-fibrogenic gene expressions in HSC-T6 were suppressed in
138 malized but the lung fibrotic abnormalities, fibrogenic gene induction and pulmonary elasticity were
139 langiocytes and activates transcription of a fibrogenic gene program that supports biliary fibrosis.
140 ), whose depletion upon activation induces a fibrogenic gene program.
141 promote fibrogenesis through coregulation of fibrogenic gene targets.
142 netic machinery in cholangiocytes to support fibrogenic gene transcription.
143 6 in liver injury may allow de-repression of fibrogenic genes and decreased stellate cell clearance b
144  direct transcriptional repression of target fibrogenic genes and increased apoptosis of activated HS
145  not improve insulin resistance, but induced fibrogenic genes and inflammation in the liver.
146 ) HSCs were unable to increase expression of fibrogenic genes IL-1beta and tissue inhibitor of metall
147       Autophagy also regulated expression of fibrogenic genes in embryonic, lung, and renal fibroblas
148 y amplifying the expression of HCV-dependent fibrogenic genes in HSC.
149  mRNA expression of pro-inflammatory and pro-fibrogenic genes in livers of CDAA rats.
150 ure resulted in upregulation (>1.9x) of five fibrogenic genes including CCL2, IL1A, IL1B, IL13RA2 and
151 s, but did not demonstrate the inhibition of fibrogenic genes observed in pn.
152 he chromatin environment of inflammatory and fibrogenic genes through its atypical histone acetyltran
153  regression of liver fibrosis, down-regulate fibrogenic genes, and acquire a phenotype similar to, bu
154 H incidence and inductions of progenitor and fibrogenic genes, but rather enhances the Il-17a inducti
155 hepatic fibrosis, with reduced expression of fibrogenic genes, compared to WT mice.
156 drial DNA deletions, and renal expression of fibrogenic genes, including transforming growth factor b
157 minished fibrosis with reduced expression of fibrogenic genes.
158  a significant increase in hepatic mRNAs for fibrogenic genes.
159 on of stellate cells and expression of human fibrogenic genes.
160 yses to identify translational regulators of fibrogenic genes.
161 several proinflammatory, cancer-related, and fibrogenic genes.
162  play an important role in the production of fibrogenic growth factors and development of fibrosis.
163 e resulting offspring better adapt to future fibrogenic hepatic insults.
164                            Effects of LPS on fibrogenic hepatic stellate cells (HSCs) from WT and TLR
165                          Here we report that fibrogenic hepatic stellate cells (HSCs) in the liver ar
166       Thus, XBP1-mediated UPR contributes to fibrogenic HSC activation and is functionally linked to
167       HSCs were isolated 24 hours later, and fibrogenic/inflammatory parameters were analyzed.
168          GIV is expressed in the liver after fibrogenic injury and is required for HSC activation.
169 tigating hepatic steatosis and in modulating fibrogenic injury and reversal.
170  inhibited PMC migration after intratracheal fibrogenic injury.
171 cid binding protein reveal distinct roles in fibrogenic injury.
172      Our previous study showed that isolated fibrogenic lung fibroblasts have high endogenous levels
173 lved hepatic inflammation, activation of the fibrogenic machinery and early fibrosis.
174 tion, and caused substantial increase in the fibrogenic marker miR-21 expression, indicating the high
175 scle actin staining and expression levels of fibrogenic markers (eg, transforming growth factor-beta1
176 ture, paralleling the enhanced expression of fibrogenic markers alpha-smooth muscle actin (alpha-SMA)
177  AR also induced marked upregulation of hHSC fibrogenic markers and reduced hHSC death.
178 ion of Rev-erbalpha, decreased expression of fibrogenic markers and the activated phenotype in HSCs,
179 uced HSC proliferation and expression of pro-fibrogenic markers of mouse and human HSCs.
180 y, and monophosphoryl lipid A down-regulated fibrogenic markers, but elicited very weak inflammatory
181 aHSCs associated with down-regulation of key fibrogenic mechanisms and thus may have an important rol
182 ng growth factor-1 (TGF-beta1) activates pro-fibrogenic mechanisms have been extensively studied and
183 dystrophy (DMD) patients, yet the implicated fibrogenic mechanisms remain poorly understood.
184      This reflects its capacity to stimulate fibrogenic mediators and induce the expression of other
185 as betaTRCP-dependent degradation of the pro-fibrogenic mediators Sp1, TAZ and beta-catenin.
186 igate the expression of the inflammatory and fibrogenic mediators which may be involved.
187 viously discovered that the IPF lung harbors fibrogenic mesenchymal progenitor cells (MPCs) that serv
188                                        These fibrogenic mesenchymal progenitors and their progeny rep
189 ignificantly increased fibrosis and enhanced fibrogenic messenger RNA (mRNA) and protein expression.
190 ted transcriptional program leading to a pro-fibrogenic microenvironment, activation of hepatic stell
191 l cell coverage fostered the accumulation of fibrogenic molecules and the attraction of fibroblasts t
192   We have therefore been able to convert pro-fibrogenic myofibroblasts in the liver into hepatocyte-l
193 ic stellate cells or portal fibroblasts into fibrogenic myofibroblasts.
194 hese findings indicate that T-cell-regulated fibrogenic pathways are highly mechanoresponsive and sug
195                  Over time, inflammation and fibrogenic pathways become dominant while in advanced di
196 y and the development of therapies targeting fibrogenic pathways hold promise for the future.
197                                              Fibrogenic pathways in the liver are principally regulat
198 at altered chitin clearance could exacerbate fibrogenic pathways in the setting of lung diseases char
199 s reveals intra-scar activity of several pro-fibrogenic pathways including TNFRSF12A, PDGFR and NOTCH
200  cardiac fibrosis via regulation of multiple fibrogenic pathways.
201 of genes involved in immune responses and in fibrogenic pathways.
202 ss-talk regulating cell fate-determining and fibrogenic pathways.
203 drive fibrogenesis by modulating the HSC pro-fibrogenic phenotype and Collagen-I expression.
204 aded cRGDyK-liposomes markedly inhibited the fibrogenic phenotype in bile duct ligation- or thioaceta
205 e pathogenesis of fibrosis by regulating the fibrogenic phenotype of hepatic stellate cells (HSCs).
206 he induced cellular responses that drive the fibrogenic phenotype remain to be elucidated.
207          The key mediators of the fibroblast fibrogenic phenotype were characterized using a novel as
208 om mice infected with B. abortus displayed a fibrogenic phenotype with patches of collagen deposition
209  cell populations, promotes their shift to a fibrogenic phenotype, and modulates sarcopenia.
210 ells could be turned into an inflammatory or fibrogenic phenotype.
211  promoted satellite cells to switch toward a fibrogenic phenotype.
212 y (M1 cells) as well as antiinflammatory and fibrogenic phenotypes (M2 cells); they affect transplant
213 el alternative splice form that modifies the fibrogenic potential of HSCs.
214 arker miR-21 expression, indicating the high fibrogenic potential of this specific carbon nanotube ty
215  indicating increased activation of HSCs and fibrogenic potential.
216 king poor cardiac lymphatic transport to the fibrogenic process and discussing potential avenues for
217 iscusses the role of nicotine in the general fibrogenic process that governs fibrosis and fibrosis-re
218 st activation, the key cell type driving the fibrogenic process, are essential to develop new therape
219 oblasts to myofibroblasts, a hallmark of the fibrogenic process, using pulmonary fibroblasts isolated
220 ulates HSC activation and inhibits the liver fibrogenic process.
221 rgan-resident, mesenchymal precursors in the fibrogenic processes in human adult lungs.
222  transmembrane protein Cx43 has key roles in fibrogenic processes including inflammatory signaling an
223 ay simultaneously block the inflammatory and fibrogenic processes of PF.
224 xpression is shown to impair TGF-beta-driven fibrogenic processes, including cell proliferation and p
225 ith Lonidamine decreased TGF-beta-stimulated fibrogenic processes, including profibrotic gene express
226 d with various immune, hepatoprotective, and fibrogenic processes.
227 are active participants in wound healing and fibrogenic processes.
228  protects against organ fibrosis by removing fibrogenic products of lipid peroxidation.
229                                Targeting the fibrogenic progenitor response represents a promising st
230 A miR-21 as a long-term memory keeper of the fibrogenic program in MSCs.
231 perglycemia-induced epigenetic activation of fibrogenic program in the kidney.
232 HSC FA utilization and in turn regulates the fibrogenic program.
233  was sufficient to confer protection against fibrogenic progression.
234                                Within days a fibrogenic, proliferative mechanism causes anatomic clos
235  differentiation trajectory IPF MPCs acquire fibrogenic properties, we analyzed the transcriptome of
236 tenuated hypoxia-induced upregulation of the fibrogenic protein connective tissue growth factor and c
237 nt autocrine signalling that is required for fibrogenic protein synthesis.
238 s well as the induction of the lipogenic and fibrogenic proteins, are completely blocked in the prese
239 vels and diminished liver expression of anti-fibrogenic receptor CB2.
240 e signaling between an immune cytokine and a fibrogenic receptor.
241                  RelA-P-Ser536 may be a core fibrogenic regulator of fibroblast phenotype.
242 tension (PH) and heart failure (HF) includes fibrogenic remodeling associated with the loss of pulmon
243 taminase 2 (TG2) as a participant in adverse fibrogenic remodeling.
244                           On the other hand, fibrogenic resolution after CCl(4) administration was im
245 iferation using anti-TWEAK antibody prevents fibrogenic response and augments fibrotic liver regenera
246 p-regulation of Rev-erbalpha is an intrinsic fibrogenic response characterized by cytoplasmic accumul
247 inhibited and is tightly associated with the fibrogenic response during severe liver damage.
248 ns, which could help explain the exaggerated fibrogenic response in IPF.
249 ar VEGF deprivation induces degeneration and fibrogenic response in retina.
250                                          The fibrogenic response in tissue-resident fibroblasts is de
251 fat overload which promotes inflammatory and fibrogenic response similar to those observed in patient
252  did not affect immune cell migration or the fibrogenic response to chronic liver injury.
253 tic sinusoidal cells are known actors in the fibrogenic response to injury.
254 lagen are targets for regulating the initial fibrogenic response to liver damage.
255        Systemic VEGF overexpression led to a fibrogenic response within the liver and was associated
256 K) activity and disrupts key features of the fibrogenic response.
257 genitor (oval) cell compartment and a severe fibrogenic response.
258 o the understanding of the TGF-beta-mediated fibrogenic response.
259 ole of pancreatic acinar cells in initiating fibrogenic responses during the early stages of alcoholi
260 yte-derived OPN and recombinant OPN promoted fibrogenic responses in HSCs (P < 0.05); neutralizing OP
261 el of AGEs, and improved proinflammatory and fibrogenic responses in mice on a high AGEs diet.
262 signaling in liver fibrosis, we compared the fibrogenic responses of wild-type (WT) and tpl2(-/-) mic
263 o RNAi-mediated silencing of CCN1 attenuates fibrogenic responses to bleomycin-induced lung injury.
264  signaling in fibroblasts and contributes to fibrogenic responses to lung injury.
265 planted mesenchymal cells, Wnt-3a stimulated fibrogenic responses while suppressing adipogenesis.
266 s off a complex sequence of inflammatory and fibrogenic responses.
267  and immunoblotting were performed to assess fibrogenic responses.
268 ardin-related transcription factor (MRTF), a fibrogenic RHOA effector, and elevated expression of con
269                                To screen the fibrogenic risk factor of specific types of MWCNT, we de
270 Here, we demonstrate key determinants of the fibrogenic set point of cardiac fibroblasts (CFs) by foc
271       Given the importance of TGF-beta1 as a fibrogenic signal, a microsystem with integrated biosens
272 ge CD36 is a critical regulator of oxidative fibrogenic signaling and that CD36-mediated phagocytosis
273  the SM alpha-actin cytoskeleton and classic fibrogenic signaling cascades, but also emphasize the re
274                                          The fibrogenic signaling events downstream of TLRs on Kupffe
275 ients, tumor fibrosis and angiotensin-driven fibrogenic signaling have been shown to inversely correl
276 dative stress, unfolded protein response and fibrogenic signaling.
277 lizes transactivation mechanisms to initiate fibrogenic signaling.
278 F), which serves as a central hub within the fibrogenic signalling network initiated by diverse class
279 chanism that regulates cardiomyocyte-derived fibrogenic signals and cardiac transcriptional pathways
280 hepatocytes produce hepato-inductive and pro-fibrogenic signals at the levels sufficient to shape the
281                                              Fibrogenic signals drive transcription of procollagen I,
282 ance activation of HSCs and induction of the fibrogenic signals in these cells.
283                     Hypothesizing that early fibrogenic signals may originate in cells susceptible to
284 eam of TGFbeta that mediate transcription of fibrogenic signals.
285 e regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of
286 iologic Epo-producing state and a pathologic fibrogenic state in response to microenvironmental signa
287 responsiveness of reverted HSCs to recurring fibrogenic stimulation.
288 eactivate into myofibroblasts in response to fibrogenic stimuli and strongly contribute to liver fibr
289 fully characterized, we aimed to analyze the fibrogenic stimuli in a new in vitro model of NASH.
290 egenerate hepatocytes in various contexts of fibrogenic stimuli remain elusive.
291 ions direct the cellular response of HPCs to fibrogenic stimuli, but also identify novel potential th
292 llular matrix organization and is induced by fibrogenic stimuli.
293 ate, with higher levels of responsiveness to fibrogenic stimuli.
294 kin, predominantly in the adipogenic but not fibrogenic subsets.
295 al cells toward myofibroblasts by inducing a fibrogenic transcriptional program while suppressing adi
296 TNF-alpha production as well as induction of fibrogenic transcripts.
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                                       During fibrogenic transition, these miRNAs are transcriptionall
300 ional repressor activity was not affected by fibrogenic treatments.

 
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