ライフサイエンスコーパス: profibrotic

1 , the data indicate that TGF-beta exerts its profibrotic action in vitro and in vivo via inactivation

2 but critically important contribution to the profibrotic activities of LPA by driving MRTF-dependent

3 t endogenous Hic-5 suppresses senescence and profibrotic activities of myofibroblasts by down-regulat

4 growth factor beta (TGFbeta) has significant profibrotic activity both in vitro and in vivo.

5 TGF-beta has potent profibrotic activity in vitro and has long been implicat

6 le the TAT-SNX9 peptide prevented TGF-beta's profibrotic activity in vitro as well as in 2 murine tre

7 pericytes, but domain 4 showed the broadest profibrotic activity.

8 nstream target of TGF-beta that mediates its profibrotic activity.

9 omerular injury; decreased the expression of profibrotic and fibrotic components, including fibronect

10 aR differentially inhibited bacteria-induced profibrotic and inflammatory mediator production by peri

11 ist Gremlin-1, and we show that Gremlin-1 is profibrotic and is mediated through canonical TGF-beta s

12 nced ROS production, increased expression of profibrotic and proinflammatory mediators, and increased

13 rstitial myofibroblast activation, including profibrotic and proinflammatory paracrine signals secret

14 ed that diabetes promoted a proinflammatory, profibrotic, and dysfunctional alternatively activated m

15 IL-13 is profibrotic, and it is released in a higher amount in pa

16 rpose of this study was to determine whether profibrotic biomarkers accurately reflect the presence a

17 U-IRI revealed high-level expression of the profibrotic BRP-39 receptor Ptgdr2/Crth2 and expression

18 erging data indicating a role for T cells in profibrotic cardiac repair and healing after ischemia, l

19 ne type-1 (MT1) MMP, may also be involved in profibrotic cascades through hydrolysis of latency-assoc

20 nobufagenin binding to Na/K-ATPase initiates profibrotic cell signaling, and heightened marinobufagen

21 cyte-derived fibrocyte, a collagen-secreting profibrotic cell.

22 mesenchymal stem cells or human hepatogenic profibrotic cells activated by transforming growth facto

23 ibrosis is a common disease process in which profibrotic cells disturb organ function by secreting di

24 signaling opposes adipogenesis and generates profibrotic cells instead, which leads to fibrotic WAT i

25 sociated with metabolic dysfunction, but how profibrotic cells originate is still being elucidated.

26 esenchymal stem cells, and human hepatogenic profibrotic cells.

27 ses them to transition into ECM-synthesizing profibrotic cells.

28 Sarcomere mutations seem to induce profibrotic changes before left ventricular hypertrophy

29 IL-18 induces profibrotic changes in TECs independent of TGF-beta1 act

30 L13/IL4-inducible skin signature wherein the profibrotic chemokine CCL2 plays a key role.

31 number of myofibroblasts, the expression of profibrotic chemokines and cytokines, and the number of

32 ed matrilytic activity, and retention of the profibrotic cleavage substrates tissue transglutaminase

33 Cells were cultured on profibrotic conditions including stiff substrata and TGF

34 d externalization of TG2, thereby preventing profibrotic crosslinking of extracellular matrix and rec

35 kidney tissue mass, collagen deposition, and profibrotic cytokine expression in two independent renal

36 +)CD28(-) T cells produce high levels of the profibrotic cytokine IL-13, which induces collagen produ

37 fibrosis, a central mediator of which is the profibrotic cytokine TGF-beta.

38 n aorta, and increased the expression of the profibrotic cytokine TGF-beta1 in aortic endothelial cel

39 ocal adhesion adaptor protein induced by the profibrotic cytokine TGF-beta1.

40 IL-6 is a profibrotic cytokine that is elevated in the prototypic

41 The profibrotic cytokine transforming growth factor beta 1 (

42 in primary MCs, and was up-regulated by the profibrotic cytokine transforming growth factor-beta1 an

43 remodeling by promoting paracrine release of profibrotic cytokine, TGFbeta1 from cardiomyocytes.

44 p-regulated the expression of CTGF, a potent profibrotic cytokine.

45 accelerated secretion of proinflammatory and profibrotic cytokines (interleukin-2, interferon-gamma,

46 acoid feedback inhibition of proinflammatory/profibrotic cytokines by T cell-derived CD73.

47 We demonstrate increased collagen and profibrotic cytokines in TLR3 knockout mice (tlr3(-/-))

48 mediators and induce the expression of other profibrotic cytokines such as platelet-derived growth fa

49 ta1 stimulated G2/M arrest and production of profibrotic cytokines that had the capacity to stimulate

50 ocyte expression of both proinflammatory and profibrotic cytokines was significantly higher in mdx(5c

51 ial cell cycle G2/M arrest and production of profibrotic cytokines were both attenuated.

52 l sources and release of proinflammatory and profibrotic cytokines, and a manifestation of organ dysf

53 ttenuated expression of monocyte chemokines, profibrotic cytokines, and collagen in aorta of mice aft

54 reous showed upregulation of T-cell markers, profibrotic cytokines, and cytokines downstream of mTOR

55 eover, we detected reduced concentrations of profibrotic cytokines, including transforming growth fac

56 ol efflux and down-regulated proinflammatory/profibrotic cytokines, inhibiting the pathomorphology of

57 Both antigen-specific CD8(+) T cells and profibrotic cytokines, such as TNFalpha and IL-13, are e

58 d interacts in a complex manner with 2 other profibrotic cytokines, TGFbeta and IL-13, strongly sugge

59 and the accumulation of proinflammatory and profibrotic cytokines.

60 which contribute to the disease by secreting profibrotic cytokines.

61 sis that HIF-1alpha mediates albumin-induced profibrotic effect in cultured renal proximal tubular ce

62 everal renal diseases, with some miRs having profibrotic effects and others having opposing effects.

63 d the mechanism by which TGF-beta exerts its profibrotic effects and specifically the role of AMP-act

64 e HIF-1alpha, which mediates albumin-induced profibrotic effects in renal tubular cells.

65 ced endothelial NOX2 activation has profound profibrotic effects in the heart in vivo that lead to a

66 The main mechanism of TSLP profibrotic effects is not as yet fully understood, alth

67 y cell NOX2 per se was not essential for the profibrotic effects of AngII.

68 Profibrotic effects of aristolochic acid are linked to g

69 apeutic dosage, is capable of inhibiting the profibrotic effects of IPF LFs and attenuates bleomycin-

70 From a clinical perspective, the profibrotic effects of PDGF-CC outweigh the pro-angiogen

71 es and primary cells and is required for the profibrotic effects of TGF-beta.

72 reversed these changes, suggesting that the profibrotic effects of TGF-beta1 are, at least in part,

73 We found that DMF blocks the profibrotic effects of transforming growth factor-beta (

74 '-diphosphate (UDP)] have been shown to have profibrotic effects, as well.

75 llenge and the IL-2 complex had no effect on profibrotic (eg, transforming growth factor-beta) or typ

76 xpression of Cu,Zn-SOD in mice resulted in a profibrotic environment and accelerated the development

77 the genetic deletion of MARCO attenuated the profibrotic environment and pulmonary fibrosis in mice e

78 translocation, might be a sign of a diseased profibrotic epithelial phenotype.

79 arget genes expressed in the skin, including profibrotic extracellular matrix collagens.

80 Mechanistically, the profibrotic factor TGF-beta1 induced hypermethylation an

81 lpha), hypertrophic factors (e.g., ANP), and profibrotic factors (e.g., TGFbeta1) from both VCM and v

82 al transition express several other secreted profibrotic factors and are capable of activating lung f

83 nd CGRP induced apoptosis and the release of profibrotic factors capable of stimulating the different

84 s a key role in epigenetic regulation of key profibrotic factors in diabetes.

85 e results identify M-CSF and IL-34 as potent profibrotic factors in HCV liver fibrosis.

86 Injury-induced epithelial secretion of profibrotic factors is hypothesized to underlie this lin

87 vitro treatment of IPF fibroblasts with the profibrotic factors TGF-beta1 or tumor necrosis factor a

88 g those of Tgfb1, Tgfb3, and Ctgf, the major profibrotic factors that are known to drive diabetic ren

89 expression of a specific subset of paracrine profibrotic factors, including Lcn2, Pdgfb, and Timp1.

90 itochondria depolarization and expression of profibrotic factors.

91 rocyte-neuronal communication in response to profibrotic factors.

92 ctions in a reciprocal manner, acting on the profibrotic family member CCN2 to inhibit fibrosis in a

93 e a therapeutic target to short-circuit this profibrotic feedback loop.

94 AR dependent, fibrotic matrix-selective, and profibrotic fibroblast phenotype may be amenable to targ

95 ice have linked high expression of CD26 to a profibrotic fibroblast phenotype, but this has not been

96 in differentiation of pluripotent cells into profibrotic fibroblasts and the potential for C-82 with

97 of transforming growth factor-beta-mediated profibrotic fibronectin, collagen I, and proinflammatory

98 Our results suggest a novel profibrotic function for IL-17A by enhancing the respons

99 regulatory role of microRNA (miR)-155 in the profibrotic function of murine lung macrophages and fibr

100 chondrially targeted antioxidants attenuated profibrotic gene expression in both normal and fibrotic

101 essive TGF-beta signaling can lead to robust profibrotic gene expression in fibroblasts, resulting in

102 Overexpression of JAK2 led to increased profibrotic gene expression in LX2 cells, which was bloc

103 ial fibrosis and attenuates hypertrophic and profibrotic gene expression in mice harboring heterozygo

104 formation of endothelial cells and decreased profibrotic gene expression in TGF-beta-stimulated fibro

105 ate the role of PDGFRalpha on proliferation, profibrotic gene expression, and migration in primary hu

106 ased LV cardiomyocyte size, hypertrophic and profibrotic gene expression, and upregulation of LV supe

107 n and LX2 cells, AG490 blocked AngII-induced profibrotic gene expression.

108 d ROS production attenuated TGF-beta-induced profibrotic gene expression.

109 ice was analyzed by histology, collagen, and profibrotic gene expression.

110 enuated the diabetes-induced upregulation of profibrotic gene markers, fibronectin and transforming-g

111 helium resulted in upregulated expression of profibrotic genes and TIF.

112 s associated with an increased expression of profibrotic genes and transforming growth factor-beta si

113 cells (HSCs), reduces expression of Gli3 and profibrotic genes but induces gfap, the inactivation mar

114 Human homologues of profibrotic genes expressed by mouse monocyte-derived al

115 Expression of collagen and profibrotic genes in aortic VSMCs increased in mice afte

116 gulated the constitutive expression of these profibrotic genes in IPF fibroblasts.

117 1(-/-) mice, and overexpression of fetal and profibrotic genes occurred only in Cav3.1(-/-).

118 that mEVs are enriched for miRs that target profibrotic genes up-regulated in IPF fibroblasts.

119 -induced upregulation of proinflammatory and profibrotic genes was significantly greater in the kidne

120 In addition, expression of these profibrotic genes was significantly higher in the cocult

121 uptake, upregulation of proinflammatory and profibrotic genes, and development of fibrosis in respon

122 modeling in Pirb(-/-) eosinophils, including profibrotic genes, genes promoting epithelial-to-mesench

123 us Red staining and increased mRNA levels of profibrotic genes, including connective tissue growth fa

124 SC activation entails enhanced expression of profibrotic genes, increase in proliferation, and increa

125 or indirectly by synergistically stimulating profibrotic genes, or production of these cytokines.

126 a1-induced SMAD3 activation and induction of profibrotic genes, supporting a positive feedback loop l

127 alveolar macrophages in their expression of profibrotic genes.

128 osis), and expression of proinflammatory and profibrotic genes.

129 ription factors regulating expression of the profibrotic genes.

130 nd wound closure and modulated expression of profibrotic genes.

131 gram that results in increased expression of profibrotic genes.

132 a low level of collagens but a high level of profibrotic growth factors as compared with i.m. fibrobl

133 Fibrocyte expression of collagens and profibrotic growth factors was not increased in Ccr2(-/-

134 tly fewer macrophages, reduced expression of profibrotic growth factors, and decreased accumulation o

135 m a quiescent state partially in response to profibrotic growth factors.

136 ocal bioavailability of antihypertrophic and profibrotic growth factors.

137 In summary, LXA4 attenuated profibrotic HLMF activity and promoted HLMF regression t

138 progression and tissue remodeling and can be profibrotic in certain conditions.

139 MI altered leaflet adaptation, including a profibrotic increase in valvular cell activation, CD45-p

140 rmal skin fibroblasts, mimicking the typical profibrotic keloid profile.

141 ariant proteins lead to the secretion of the profibrotic latent transforming growth factor (TGF)-beta

142 iated with augmented liver production of the profibrotic lectin, galectin-3.

143 The profibrotic ligands TGF-beta and angiotensin II induced

144 tor for asbestos, polarizes macrophages to a profibrotic M2 phenotype, and is required for the develo

145 ulator in driving an alternatively activated profibrotic macrophage phenotype in UUO-induced CKD.

146 rat epoxygenase Cyp2j4 as a determinant of a profibrotic macrophage transcriptome that could have imp

147 the differentiation of human monocytes into profibrotic macrophages (Mphi) remain poorly defined.

148 ression of E-cadherin and an increase in the profibrotic markers alpha-smooth muscle actin (alpha-SMA

149 nger RNA levels; decreased the expression of profibrotic markers during wound healing; decreased ROS

150 ferentiation decreased the expression of the profibrotic markers fibronectin and hypoxia-inducible fa

151 ced albuminuria, and inhibited expression of profibrotic markers in animal models with lupus nephriti

152 -KG restored TGF-beta1-induced expression of profibrotic markers in GLS1-deficient myofibroblasts.

153 ndothelial dysfunction and the expression of profibrotic markers in the heart.

154 receptor Ptgdr2/Crth2 and expression of the profibrotic markers Lgals3, Pdgfb, Egf, and Tgfb In comp

155 sed expression levels of proinflammatory and profibrotic markers that were independent of glycemic an

156 ib significantly reduced the upregulation of profibrotic markers, phosphorylation of Smad3, and renal

157 lized to HSC and increased the expression of profibrotic markers.

158 and inhibited mRNA expression of a number of profibrotic markers.

159 nd reduced expression of proinflammatory and profibrotic markers.

160 n, abrogated TGF-beta1-induced expression of profibrotic markers.

161 lpha targets progenitor cell plasticity as a profibrotic mechanism.

162 -derived growth factor (PDGF)-CC as a potent profibrotic mediator in kidney fibrosis and pro-angiogen

163 tify soluble ephrin-B2 (sEphrin-B2) as a new profibrotic mediator in lung and skin fibrosis.

164 Galectin-3, a profibrotic mediator, is linked to the development of re

165 sence of CX3CR1 and produced more of the key profibrotic mediator, TGF-beta.

166 knockdown of FKBP10 attenuated expression of profibrotic mediators and effectors, including collagens

167 umulated in organized clusters and expressed profibrotic mediators at >/=25 wk after irradiation (fib

168 re associated with reduced expression of the profibrotic mediators, transforming growth factor-beta1

169 AMs, cell differentiation, and production of profibrotic mediators.

170 ween HA, CD73/adenosine signaling, and other profibrotic mediators.

171 itor 1B (p27Kip1) and of proinflammatory and profibrotic mediators.

172 renal mRNA expression of proinflammatory and profibrotic mediators.

173 cluding cell proliferation and production of profibrotic mediators.

174 ) injury is a key step that contributes to a profibrotic microenvironment.

175 neration, but chronic inflammation creates a profibrotic milieu that exacerbates disease progression.

176 etic db/db mice significantly down-regulates profibrotic miRNA-155 in the myocardium and improves LV

177 p, miR-132, and miR-212) and upregulation of profibrotic miRNAs (miR-142, and miR-147).

178 es and lung parenchymal cells are sources of profibrotic MMP-8 during bleomycin-mediated lung fibrosi

179 sion of ion channel proteins in myocytes and profibrotic molecules in nonmyocyte cells that are impor

180 iR-150 promotes renal fibrosis by increasing profibrotic molecules through downregulation of SOCS1.

181 ecretion of a variety of proinflammatory and profibrotic molecules.

182 F-beta in lung myofibroblasts and a distinct profibrotic myofibroblast phenotype driven by stimulatio

183 Deletion of GSK-3beta induces a profibrotic myofibroblast phenotype in isolated cardiac

184 everity and form part of a TGF-beta1-induced profibrotic network.

185 verse relationship between cell division and profibrotic ontologies associated with reduced basic fib

186 t converts vasculoprotective pantethine into profibrotic pantothenic acid and pro-oxidant cystamine,

187 etinas, whereas there was an upregulation of profibrotic pathway mediated by transforming growth fact

188 y in epithelial cells, lead to activation of profibrotic pathways in epithelial cells.

189 significantly attenuated TGF-beta1-mediated profibrotic pathways in vitro and in vivo, while esculet

190 and we conclude with a summary of how these profibrotic pathways may be interrelated.

191 mmatory, pro-oxidative, vasoconstrictor, and profibrotic pathways may contribute to adverse outcomes

192 Activation of these profibrotic pathways was additive following HIV/HCV coex

193 smetabolism, NAFLD and fibrosis, analysis of profibrotic pathways, liver innate immune cells, and rea

194 s associated with genes involved in multiple profibrotic pathways, where BRD4 is colocalized with pro

195 ischaemia propensity, and the activation of profibrotic pathways.

196 gnaling increases that trigger production of profibrotic peptides, proliferation of interstitial fibr

197 vascular endothelial growth factor but more profibrotic peptides.

198 MCU expression polarized macrophages to a profibrotic phenotype after exposure to asbestos, and th

199 red for the polarization of macrophages to a profibrotic phenotype as mutation of these residues redu

200 transition (MesoMT), whereby they acquire a profibrotic phenotype characterized by increased express

201 roblasts (SFBLs), and this associates with a profibrotic phenotype distinct from gingival fibroblasts

202 ese genes play a key role in determining the profibrotic phenotype in SSc fibroblasts.

203 , enforced expression of miR-155 reduced the profibrotic phenotype of IPF and miR-155(-/-) fibroblast

204 Retinoid overload helps explain the profibrotic phenotype of Lxralphabeta(-/-) mice, and we

205 The profibrotic phenotype of SFBLs partially depended on exp

206 mal human lung fibroblasts recapitulates the profibrotic phenotype seen in FRNK-deficient cells.

207 d human and mouse lung fibroblasts induced a profibrotic phenotype, whereas treating human fibroblast

208 acrophages toward an alternatively activated profibrotic phenotype, which promotes collagen productio

209 Carbon monoxide reversed this IPF PMC profibrotic phenotype.

210 reas the CD11b(+)/Ly6C(low) population had a profibrotic phenotype.

211 pression in vivo and in vitro reverses these profibrotic phenotypes.

212 and its loss as observed in IPF facilitates profibrotic phenotypic changes.

213 Once expressed, GIV enhances the profibrotic (PI3K-Akt-FoxO1 and TGFbeta-SMAD) and inhibi

214 Profibrotic polarization was abrogated when MCU was abse

215 henotype after exposure to asbestos, and the profibrotic polarization was regulated by MCU-mediated A

216 ess higher amounts of MARCO and have greater profibrotic polarization.

217 lize the mitochondrial calcium uniporter for profibrotic polarization.

218 ed the expression and production of numerous profibrotic/proinflammatory cytokines, chemokines, and g

219 HSCs transdifferentiation, characterized by profibrotic properties and collagen modification, with s

220 We next analyzed the acquisition of profibrotic properties by Mphi generated with M-CSF (M-C

221 erentiation of monocytes/macrophages and has profibrotic properties, modulates wound healing and remo

222 creased expression of SOCS7, and increase in profibrotic proteins and miR-199a-3p.

223 cytokine signaling 1 (SOCS1) and upregulated profibrotic proteins in both proximal tubular and mesang

224 0 expression, decreased SOCS1, and increased profibrotic proteins in proximal tubular cells and podoc

225 d platelet-derived growth factor, as well as profibrotic proteins such as galectin-3.

226 ectly suppressing proinflammatory cytokines, profibrotic proteins, and proliferation of lung fibrobla

227 and promotes TGFbeta-1-induced expression of profibrotic proteins, such as fibronectin (FN) and alpha

228 TGF-beta1, reduced SOCS1, and an increase in profibrotic proteins.

229 with chronicity scores and the expression of profibrotic proteins.

230 ved nicotine on cellular functions including profibrotic response and other functional aspects is not

231 tly, JunB mediates the TGF-beta induction of profibrotic response factors, fibronectin, fibulin-2, tr

232 human skin but not in gingiva may drive the profibrotic response leading to excessive scarring.

233 This proinflammatory profibrotic response might be a key cause of inflammatio

234 Here, we investigated the role of BRP-39 in profibrotic responses after AKI.

235 Subsequent profibrotic responses are shown to involve the cooperati

236 The regulation of profibrotic responses by canonical Wnt/beta-catenin was

237 elease activates P2Y(2) receptors to mediate profibrotic responses in CFs, implying that nucleotide r

238 a critical role of TAZ/YAP in mediating the profibrotic responses in dermal fibroblasts.

239 sociation of Brd4 with genes involved in the profibrotic responses in IPF LFs as demonstrated using c

240 contributors to tissue fibrosis, we compared profibrotic responses in wild-type and Ptpra(-/-) mouse

241 We investigated the role of Brd on the profibrotic responses of lung fibroblasts (LFs) in patie

242 R2, TLR4, or the coreceptor CD14 reduced the profibrotic responses of uremic leukocytes to endogenous

243 g the transcriptional program of the EMT and profibrotic responses to TGF-beta.

244 These profibrotic responses were abrogated by both genetic and

245 t its up-regulation may augment high glucose profibrotic responses.

246 ndicating a role of the cytokine IL-1beta in profibrotic responses.

247 ator of lung fibrosis by repressing multiple profibrotic responses.

248 nhibited PDE-induced, TLR2- or TLR4-mediated profibrotic responses.

249 ic overexpression of ATX established a liver profibrotic role for ATX/LPA, whereas pharmacological AT

250 h reduced levels of MCP-1, consistent with a profibrotic role for native KIM-1.

251 has been tempered by concerns of a possible profibrotic role of endogenous MSCs in response to injur

252 on after ureteral obstruction is the primary profibrotic signal and that renal denervation prevents b

253 t, unregulated, and progressively increasing profibrotic signaling along multiple pathways.

254 vestigated the role of TGF-beta1 in inducing profibrotic signaling from epithelial cells to activate

255 tein CCN1 enhances TGF-beta1/SMAD3-dependent profibrotic signaling in fibroblasts and contributes to

256 dia of BMPC inhibited miR-155 expression and profibrotic signaling in mouse cardiac fibroblasts under

257 or of macrophage-myofibroblast crosstalk and profibrotic signaling in the setting of maladaptive kidn

258 t signaling pathway to drive contraction and profibrotic signaling in these cells.

259 ffects of these cytokines on contraction and profibrotic signaling pathways in fibroblasts from the p

260 We conclude that PTP-alpha promotes profibrotic signaling pathways in fibroblasts through co

261 y should lead to mechanistic studies on TSLP profibrotic signaling.

262 tion of transforming growth factor-dependent profibrotic signaling.

263 on of RhoA, which is known to be involved in profibrotic signalling pathways.

264 mediate tissue inflammation, cell death and profibrotic signalling.

265 STAT3 thus integrates several profibrotic signals and might be a core mediator of fibr

266 a multiple receptor-driven process in which profibrotic signals are enhanced and antifibrotic pathwa

267 Here we show that profibrotic signals converge on STAT3 and that STAT3 may

268 ion, associated with decreased expression of profibrotic signals TGF-beta1, CCN2 and ET-1, downstream

269 stellate cells (HSCs), and amplification of profibrotic signals.

270 ed with the extent of abdominal fat deposit, profibrotic state (as reflected by circulating PICP), re

271 fting acute inflammation into a more chronic profibrotic state through induction of Th1 cell response

272 in bouts separated by 4 d, whereas a chronic profibrotic state was seen in bouts separated by 10 d.

273 elial-to-mesenchymal transition (EMT) to the profibrotic stiff microenvironment and myofibroblast acc

274 ion and inhibition on fibroblast response to profibrotic stimuli were analyzed in vitro in primary hu

275 reduced the responsiveness of fibroblasts to profibrotic stimuli, including significant reductions in

276 myofibroblast differentiation on exposure to profibrotic stimuli.

277 in HSCs and facilitates VDR binding at SMAD3 profibrotic target genes via TGFbeta1-dependent chromati

278 pSMAD3 using the TAT-SNX9 peptide inhibited profibrotic TGF-beta activity in murine cells and human

279 cription factors, the canonical mediators of profibrotic TGF-beta responses.

280 tives on the interrelation of metabolism and profibrotic TGF-beta signaling and present opportunities

281 early growth response 1), a key regulator of profibrotic TGF-beta signaling.

282 lities, fractionated electrograms, increased profibrotic TGF-beta1 expression, interstitial atrial fi

283 asts into myofibroblasts via suppressing the profibrotic TGF-beta1 signaling.

284 hways, including ERK and AKT, as well as the profibrotic TGF-beta1/SMAD pathway.

285 provide important mechanistic insights into profibrotic TGFbeta signaling and indicate that targetin

286 -23p19 production by hepatocytes may enhance profibrotic Th17 signaling and proinflammatory IFN-gamma

287 Volume overload LVH (VOH) is less profibrotic than pressure overload LVH (POH).

288 llowing MI may separately regulate different profibrotic traits of activated CFBs.

289 tic pathways, where BRD4 is colocalized with profibrotic transcription factors.

290 r-activated receptor-gamma levels and show a profibrotic transcriptome, displaying overexpression of

291 ith diabetic nephropathy (DN) that amplifies profibrotic transforming growth factor (TGF)-beta1 signa

292 Profibrotic transforming growth factor-beta of acinar ce

293 P1) is activated by tissue stiffness and the profibrotic transforming growth factor-beta1, but its ro

294 Mechanistically, GSK-3beta inhibits profibrotic transforming growth factor-beta1/SMAD-3 sign

295 tumor necrosis factor alpha, and F4/80) and profibrotic (transforming growth factor beta, tissue inh

296 n-allergen-driven diseases, characterized by profibrotic type 2 immune phenotypes and excessive fibro

297 Profibrotic up-regulation of glucose transporter 1 by TG

298 r a week, the cardiac environment changed to profibrotic with growth factor and TH2-interleukin synth

299 The AHR and AHR ligands block profibrotic Wnt signaling by inhibiting the phosphorylat

300 3, indicating that Klotho inhibition of the profibrotic Wnt/TGFbeta axis underlies its anti-fibrotic