ライフサイエンスコーパス: myofibroblast

1 ere to CFB, and induce their transition into myofibroblasts.

2 inflammatory cells, and their crosstalk with myofibroblasts.

3 t reprograms adipose-derived stem cells into myofibroblasts.

4 chondrocytes, osteoblasts, fibroblasts, and myofibroblasts.

5 pha-smooth muscle actin (alpha-SMA)-positive myofibroblasts.

6 migration, and collagen secretion of cardiac myofibroblasts.

7 leukocyte infiltration and activates infarct myofibroblasts.

8 and differentiated into fibroblasts and then myofibroblasts.

9 he electrophysiological phenotype of cardiac myofibroblasts.

10 ion of profibrotic markers in GLS1-deficient myofibroblasts.

11 the increased COL1A2 expression observed in myofibroblasts.

12 ntractile and extracellular matrix-producing myofibroblasts.

13 control pericyte migration and conversion to myofibroblasts.

14 tropic effect on the electrical phenotype of myofibroblasts.

15 e reactivity of AOC3 match that expected for myofibroblasts.

16 ersistent alveolar alpha-smooth muscle actin myofibroblasts.

17 ated epithelial injuries and accumulation of myofibroblasts.

18 te were observed in TGF-beta1-differentiated myofibroblasts.

19 opoietin hypermethylation are upregulated in myofibroblasts.

20 y an important role in activation of infarct myofibroblasts.

21 progression, along with the number of portal myofibroblasts.

22 from differentiated smooth muscle cells and myofibroblasts.

23 factor is important for MFG-E8 production in myofibroblasts.

24 duces fibroblasts to transdifferentiate into myofibroblasts.

25 onist SFRP4, in surgical specimen-derived DD myofibroblasts.

26 fibrosis reflecting reduced accumulation of myofibroblasts.

27 ve as a cell of origin for disease-mediating myofibroblasts.

28 ferentiation into either lens fiber cells or myofibroblasts.

29 e injury, activation, and differentiation of myofibroblasts.

30 ng wound healing, adipocytes regenerate from myofibroblasts, a cell type thought to be differentiated

31 PF through the regulation of fibroblast and myofibroblast accumulation and angiogenesis.

32 BRP-39 depletion did not affect myofibroblast accumulation but did attenuate myofibrobla

33 o the profibrotic stiff microenvironment and myofibroblast accumulation in pulmonary fibrosis remains

34 anifests with detrimental tissue remodeling, myofibroblast accumulation, and scarring in the orbit of

35 rophylactic treatment with AMA0825 inhibited myofibroblast accumulation, expression of pro-fibrotic f

36 ty and is commonly characterized by aberrant myofibroblast accumulation.

37 G-E8-mediated engulfment of apoptotic cells, myofibroblasts acquired antiinflammatory properties.

38 ocardial injury would attenuate pathological myofibroblast activation and cardiac remodeling.

39 ting factor 1 drives early monocyte-mediated myofibroblast activation and collagen deposition, subseq

40 ough the function of protein-coding genes in myofibroblast activation and fibrosis have been a topic

41 from proximal tubules displayed interstitial myofibroblast activation and proliferation and increased

42 unction; however, the molecular mediators of myofibroblast activation have yet to be fully identified

43 OCKs) play multiple roles in TGFbeta-induced myofibroblast activation that could be therapeutic targe

44 s pathologic changes regulating interstitial myofibroblast activation, including profibrotic and proi

45 mma-GRK2 inhibition in limiting pathological myofibroblast activation, interstitial fibrosis, and HF

46 ithelial and endothelial cell proliferation, myofibroblast activation, stem and tissue progenitor cel

47 ession of TGFbeta1 and genes associated with myofibroblast activation, with evidence of stromal remod

48 generation is required for TGF-beta1-induced myofibroblast activation.

49 pporting a positive feedback loop leading to myofibroblast activation.

50 ling M2 response, with newly formed vessels, myofibroblasts activation and a shift on the type of col

51 The biophysically altered dermis increased myofibroblast activity and integrin beta1/pFAK/pAKT mech

52 ntially generates pathologically deleterious myofibroblasts after injury.

53 ng several extracellular matrix proteins and myofibroblast and cell contractility-related molecules,

54 and ZM241385 treatment reduced the number of myofibroblasts and angiogenesis.

55 immunity, and most unexpectedly, generating myofibroblasts and associated wound-healing responses.

56 siology after targeted disruption of coupled myofibroblasts and by cessation of ectopic activity of c

57 nd increased gap junctional coupling between myofibroblasts and cardiomyocytes >5-fold as reflected b

58 alters the electrophysiological phenotype of myofibroblasts and cardiomyocytes and whether it affects

59 h age, cardiac fibrosis (increased number of myofibroblasts and enhanced expression and deposition of

60 cked cardiac fibroblast differentiation into myofibroblasts and ensuing fibrosis in response to ische

61 poptosis, proliferation, and accumulation of myofibroblasts and extracellular matrix deposition resul

62 ger 2 (AE2) (SLC4A2 product) was detected in myofibroblasts and fibroblasts, but not in CRC cells.

63 that stimulate mesenchymal stem cells (MSC), myofibroblasts and fibroblasts.

64 ycation by MGO stimulates differentiation of myofibroblasts and production and assembly of FN.

65 ration of fibroblasts and MSCs, formation of myofibroblasts and production of collagen matrix in woun

66 nhibition of EMT prevented the generation of myofibroblasts and production of ECM proteins during chl

67 p could induce LR-MSCs to differentiate into myofibroblasts and promote pulmonary fibrogenesis, while

68 extensive subculture or differentiation into myofibroblasts and rescue conduction slowing in an in vi

69 n these two cell types: NKX2-3 and LRRC17 in myofibroblasts and SHOX2 and TBX5 in skin fibroblasts.

70 enome microarray mRNA-expression profiles of myofibroblasts and skin fibroblasts revealed four additi

71 scription factor that drives accumulation of myofibroblasts and the development of lung fibrosis.

72 g tissue and coculture models, we found that myofibroblasts and the fibrotic microenvironment created

73 Here we investigated the origin of activated myofibroblasts and the molecular mechanisms governing fi

74 the heart and their transdifferentiation to myofibroblasts and thus attenuates cardiac fibrosis.

75 in fibrosis, collagen synthesis, numbers of myofibroblasts, and accumulation of CD4(+) lymphocytes,

76 n of physiological remodeling, activation of myofibroblasts, and formation of a fibrous scar.

77 erentiated pericytes into cytokine-producing myofibroblasts, and further activated established myofib

78 eolar fluid, resident macrophages/monocytes, myofibroblasts, and the adventitia of blood vessels in l

79 tion of the extracellular matrix, removal of myofibroblasts, and the role of inflammatory cells.

80 In healing myocardial infarction, myofibroblast- and cardiomyocyte-specific activation of

81 CCA in the hepatic PME and TME, focusing on myofibroblast- and extracellular matrix-associated growt

82 idual regenerative potential of scar-forming myofibroblasts are largely determined by their origin.

83 Myofibroblasts are not present in the normal liver but a

84 Myofibroblasts are responsible for increased collagen de

85 Fibroblasts/myofibroblasts are thought to be the major cell type inv

86 Pericytes, the precursors of myofibroblasts, are a source of pathological matrix coll

87 tion of alpha-smooth muscle actin-expressing myofibroblasts arising from interactions with soluble me

88 llagen synthesis, and perturbed alignment of myofibroblast arrays in the infarct.

89 Our results define the myofibroblast as a periostin-expressing cell type necess

90 Thus, we identify the myofibroblast as a plastic cell type that may be manipul

91 on resulted from electrotonic crosstalk with myofibroblasts as demonstrated by immediate normalizatio

92 n, and alpha-smooth muscle actin, specifying myofibroblasts as the predominant cell population underg

93 Our results show that colorectal myofibroblasts, as defined by the expression of AOC3, NK

94 rophages at the early stage and by activated myofibroblasts at the later stage.

95 identify in mouse a population of migratory myofibroblasts at the leading edge of the closing VBW th

96 -beta1 depolarized cardiomyocytes coupled to myofibroblasts by approximately 20 mV and increased gap

97 urface monoamine oxidase, as a new marker of myofibroblasts by showing that it is the target protein

98 , we discuss the functional contributions of myofibroblasts, CAFs, and fibrosis to the development of

99 In Science, Plikus et al. report that myofibroblasts can generate lipid-filled adipocytes in l

100 anges proved to be pivotal for proarrhythmic myofibroblast-cardiomyocyte crosstalk in vitro, which su

101 yocytes and whether it affects proarrhythmic myofibroblast-cardiomyocyte crosstalk observed in vitro.

102 A knockdown of NKX2-3 in myofibroblasts caused a decrease of myofibroblast-relate

103 hat NKX2-3 is a key mediator for maintaining myofibroblast characteristics.

104 st (CFB) activation and differentiation into myofibroblasts, characterized by proliferation, extracel

105 TGFbeta1/CD44V6 pathway is important in lung myofibroblast collagen-1 and alpha-smooth-muscle actin s

106 Here, we studied acid handling by myofibroblasts (colon cancer-derived Hs675.T, intestinal

107 lung fibroblasts have a higher percentage of myofibroblasts compared to wild type primary lung fibrob

108 s also increased in TGF-beta1-differentiated myofibroblasts compared with controls, whereas glutamine

109 anges in collagen alignment, skin thickness, myofibroblast content, angiogenesis, and epidermal hyper

110 ion during disease progression, they adopt a myofibroblast-contractile phenotype and secrete and conc

111 trix production, myofibroblast invasion, and myofibroblast contractility.

112 ntiation process from Sox10(+) stem cells to myofibroblasts could be recapitulated in vitro.

113 P-39 as an important activator of macrophage-myofibroblast crosstalk and profibrotic signaling in the

114 inflammatory reaction and differentiation of myofibroblasts culminate in pathologic deposition of col

115 Despite no change in fibrosis or myofibroblast density (p = 0.40), there was a 16.7-fold

116 ll, Schneider et al. report that bone marrow myofibroblasts derive from Gli1(+) mesenchymal stromal c

117 roles regulating these processes: pericrypt myofibroblast-derived Wnt-5a and the microbial metabolit

118 Myofibroblasts develop contractile functions and secrete

119 GANT61 inhibited Gli1(+) cell expansion and myofibroblast differentiation and attenuated fibrosis se

120 yl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits myofibroblast differentiation and collagen deposition ac

121 locked alpha-smooth muscle actin expression, myofibroblast differentiation and function.

122 ive molecule against RILF through inhibiting myofibroblast differentiation and inflammation.

123 ), or 4 (C terminus) independently activated myofibroblast differentiation and wound healing response

124 d that both nicotine and e-cigarette inhibit myofibroblast differentiation as shown by smooth muscle

125 We found that a high-fat diet promotes myofibroblast differentiation by decreasing microRNA 140

126 w that TGF-beta1 induces local fibroblast-to-myofibroblast differentiation in a dose-dependent fashio

127 ed fibroblast proliferation, activation, and myofibroblast differentiation in an AREG-dependent manne

128 ivity was sufficient to induce fibroblast-to-myofibroblast differentiation in primary human lung fibr

129 ty to investigate the role of dietary fat on myofibroblast differentiation in the mammary stromal mic

130 lular matrix protein production, and blocked myofibroblast differentiation in vivo in mouse lung tiss

131 Fibroblast to myofibroblast differentiation is a key process during wo

132 Myofibroblast differentiation is characterized by the ex

133 that miR-877-3p sequestration inhibited the myofibroblast differentiation of LR-MSC and attenuates b

134 eta1 signaling pathway, was decreased in the myofibroblast differentiation of LR-MSC and up-regulatio

135 pression profiles of miRNAs before and after myofibroblast differentiation of LR-MSC, we identified m

136 Myofibroblast differentiation of lung resident mesenchym

137 5p was significantly upregulated both during myofibroblast differentiation of lung resident mesenchym

138 nsduces cytokine and mechanical signals into myofibroblast differentiation through the transcription

139 causes dysregulated repair by inhibition of myofibroblast differentiation via OXPHOS pathway.

140 or treatment reduced leukocyte infiltration, myofibroblast differentiation, and fibrotic injury both

141 esized that nicotine and e-cigarettes affect myofibroblast differentiation, gel contraction, and woun

142 ne and e-cigarette condensate and determined myofibroblast differentiation, mitochondrial oxidative p

143 e NOX4/ROS production, which is required for myofibroblast differentiation, myofibroblast differentia

144 required for myofibroblast differentiation, myofibroblast differentiation, myofibroblast extracellul

145 F-beta1-induced fibroblast proliferation and myofibroblast differentiation, PMC mesothelial-to-mesenc

146 a-smooth muscle actin, alpha-SMA) markers of myofibroblast differentiation, resulting in a time cours

147 nolysis and metabolites of TCA in supporting myofibroblast differentiation.

148 xtracellular Gln prevented TGF-beta1-induced myofibroblast differentiation.

149 ffects by nicotine resulted in inhibition of myofibroblast differentiation.

150 gnaling and miR-140 downregulation-dependent myofibroblast differentiation.

151 en species (ROS) signaling that mediates the myofibroblast differentiation.

152 HC5 knockdown by siRNA confirmed its role in myofibroblast differentiation.

153 ent proliferation, motility, and indirectly, myofibroblast differentiation.

154 of TGF-beta1 signaling as well as increased myofibroblast differentiation.

155 3 variants, as well as subtle differences in myofibroblast differentiation.

156 lung immobilizes the fibroblast and promotes myofibroblast differentiation.

157 significant reductions in cell survival and myofibroblast differentiation.

158 ling, matrix remodeling, and TGFbeta-induced myofibroblast differentiation.

159 blast metabolic reprogramming that regulates myofibroblast differentiation.

160 eta1 in tumor cells also failed to result in myofibroblast differentiation.

161 r mechanisms that account for the fibroblast-myofibroblast differentiation/activation in idiopathic p

162 In this study, we found that TAM and myofibroblasts directly support chemoresistance of pancr

163 ctopic activity of cardiomyocytes coupled to myofibroblasts during pharmacological gap junctional unc

164 Yet IPF myofibroblasts exhibited higher stiffness and expression

165 myofibroblast accumulation but did attenuate myofibroblast expression of Col1a1, Col3a1, and Fn1 Toge

166 ferentiation, myofibroblast differentiation, myofibroblast extracellular matrix production, myofibrob

167 nt the excessive tissue remodeling caused by myofibroblast formation and activation.

168 A similar inhibition of myofibroblast formation and healing was also observed in

169 gate whether this pathway can directly drive myofibroblast formation and the cardiac fibrotic respons

170 which were CD8(+)), and dramatically reduced myofibroblast formation compared to control treated eyes

171 ying the stimulation of stromal fibrosis and myofibroblast formation in corneal wound healing have no

172 e marrow-derived fibroblast accumulation and myofibroblast formation in the kidneys following DOCA-sa

173 roblast to program the fibrotic response and myofibroblast formation in vivo, suggesting a novel ther

174 The canonical cytokine that induces myofibroblast formation is transforming growth factor (T

175 that AHR ligands prevent TGF-beta-dependent myofibroblast formation, and this ability is dependent o

176 ith TED were treated with TGF-beta to induce myofibroblast formation, contraction, and proliferation.

177 In addition, ITF2357 reduced myofibroblast formation, suppressed phosphorylation of S

178 This coincided with reduced cell density and myofibroblast formation.

179 found to regulate cell survival, growth and myofibroblast formation.

180 g the phosphorylation of GSK3beta to prevent myofibroblast formation.

181 ell (MSC)-like cells and bone marrow-MSCs in myofibroblast generation during fibrosis development.

182 -dependent differentiation of fibroblasts to myofibroblasts, highlighting its importance as a novel p

183 calized in subpopulations of macrophages and myofibroblasts; however, after 7 to 28 days of transvers

184 sed infiltration of EP4 expressing alpha-SMA myofibroblasts, identifying a potential mechanism of lat

185 t by epithelial dedifferentiation, increased myofibroblasts, immune cell infiltration, and increased

186 and the fibrotic microenvironment created by myofibroblasts impact the stemness and proliferation of

187 broblasts, and further activated established myofibroblasts in a manner requiring canonical and nonca

188 s promoted the proliferation of alpha-SMA(+) myofibroblasts in a paracrine manner.

189 failed to reach the values exhibited by IPF myofibroblasts in all parameters examined.

190 enesis and is upregulated in fibroblasts and myofibroblasts in disease.

191 the generation of hepatocyte-like cells from myofibroblasts in fibrotic mouse livers and reduced live

192 Better understanding of the role of myofibroblasts in HCC and CCA development and progressio

193 AOC3 was also induced in myofibroblasts in human idiopathic pulmonary fibrosis.

194 al progenitors are the predominant source of myofibroblasts in injured adult lung.

195 the contribution of cell populations to the myofibroblasts in liver fibrosis.

196 sults indicate a pivotal significance of VBW myofibroblasts in orchestrating ventral midline closure

197 ts BM-FPC homing and transdifferentiation to myofibroblasts in pressure-overloaded myocardium.

198 ults reveal previously unrecognized roles of myofibroblasts in regulating apoptotic engulfment and a

199 erivascular niche to become fibrosis-driving myofibroblasts in the bone marrow.

200 Pericryptal myofibroblasts in the colon and rectum play an important

201 n colocalized in an interface region between myofibroblasts in the focus core and normal alveolar str

202 mouse lines shows that periostin-expressing myofibroblasts in the heart derive from tissue-resident

203 herefore been able to convert pro-fibrogenic myofibroblasts in the liver into hepatocyte-like cells w

204 tellate cells, which are the major source of myofibroblasts in the liver.

205 riven transdifferentiation of fibroblasts to myofibroblasts in the presence of siRNA specific to Id3.

206 Investigating the cellular origin of myofibroblasts in various diseases is thus a promising s

207 lycistronic lentiviral vector converts mouse myofibroblasts into cells with a hepatocyte phenotype.

208 ctor-mediated reprogramming to convert liver myofibroblasts into hepatocyte-like cells in mice.

209 etaR that is highly upregulated on activated myofibroblasts, into microspheres composed of hydrophili

210 ofibroblast extracellular matrix production, myofibroblast invasion, and myofibroblast contractility.

211 The appearance of myofibroblasts is generally thought to be the underlying

212 athological intracellular mechanism in liver myofibroblasts is not completely understood, and further

213 eposition and tissue remodeling by activated myofibroblasts, leads to loss of proper tissue architect

214 revealed clonal expansion of Lkb1-deficient myofibroblast-like cell foci in the tumor stroma.

215 rmed heterogeneous populations surrounded by myofibroblast-like cells.

216 differentiation of spheres and purified the myofibroblast-like cells.

217 In both conditions, the activation of myofibroblast-like pancreatic stellate cells (PSCs) play

218 c stroma, upon activation transitioning to a myofibroblast-like, high matrix secreting phenotype.

219 aled a significant reduction in fibroblasts, myofibroblasts, macrophages, and leukocytes with a reduc

220 MFG-E8-producing myofibroblasts mainly originated from resident cardiac f

221 -beta1-induced EMT and the expression of the myofibroblast marker alpha smooth muscle actin (alphaSMA

222 eated collagen stimulated an increase in the myofibroblast marker alpha-SMA, production and assembly

223 )1a1, Col1a2, and fibronectin as well as the myofibroblast marker, alpha-smooth muscle actin.

224 morphology, stiffness, and expression of EMT/myofibroblast markers and fibrillar collagens.

225 emerging role of MSCs and MSC-like cells in myofibroblast-mediated fibrotic disease in the kidney, l

226 at glutaminolysis is a critical component of myofibroblast metabolic reprogramming that regulates myo

227 of extracellular matrix-secreting activated myofibroblasts (MFBs) in place of functional parenchymal

228 investigate the role of TGF-beta and IL-6 in myofibroblasts (MFs) - lung cancer cell interactions, lu

229 Initially, collagen produced by myofibroblasts (MFs) functions to maintain the integrity

230 og-regulated genes that enable HSC to become myofibroblasts (MFs).

231 so acts downstream of TGF-beta2 to stimulate myofibroblast migration.

232 rt, lung, and kidney as a result of enhanced myofibroblast numbers.

233 No changes in collagen transcription or myofibroblasts numbers were observed.

234 3 antibodies can be used for FACS sorting of myofibroblasts obtained by nonenzymatic procedures.

235 Wnt-5a, secreted by stromal myofibroblasts of the lower crypt, promotes proliferatio

236 cell fates: either transdifferentiating into myofibroblasts or maturing into lens fiber cells.

237 Myofibroblasts participate in physiological wound healin

238 signaling pathway as an important factor in myofibroblast perpetuation, fibrogenesis, and chronic di

239 ver, upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibros

240 aling pathways that sustain fibrosis and the myofibroblast phenotype has prevented the development of

241 All fibroblasts acquired a robust myofibroblast phenotype on TGF-beta1 stimulation.

242 novel positive-feedback loop that links the myofibroblast phenotype to TGFbeta1-stimulated CD44V6/ER

243 has been implicated in the cardiac and lung myofibroblast phenotype.

244 )) for differentiation of lung fibroblast to myofibroblast phenotype.

245 e demonstrated that activated PFs (aPFs) and myofibroblasts play a critical role in the pathogenesis

246 Activated fibroblasts (myofibroblasts) play a critical role in cardiac fibrosis

247 that EMT does not contribute directly to the myofibroblast population, and may contribute to the stif

248 tion of GRK2 in activated fibroblasts (i.e., myofibroblasts) post-I/R injury demonstrated significant

249 y-induced activation of pericytes, which are myofibroblast precursors attached to endothelial cells,

250 oblasts, suggesting that EMT does not elicit myofibroblast precursors either.

251 follicles or deletion of the BMP receptor in myofibroblasts prevented adipocyte formation.

252 Myofibroblasts previously have been distinguished from n

253 roblastic tumors (IMTs) are characterized by myofibroblast proliferation and an inflammatory cell inf

254 roma-derived R-spondin 3 produced by gastric myofibroblasts proximal to the stem cell compartment.

255 showing that it is the target protein of the myofibroblast-reacting mAb PR2D3.

256 Deletion of periostin(+) myofibroblasts reduces collagen production and scar form

257 KX2-3 in myofibroblasts caused a decrease of myofibroblast-related gene expression and increased expr

258 Myofibroblasts remain a poorly defined cell type in term

259 Myofibroblast reprogramming required neogenic hair folli

260 The myofibroblasts, responsible for extracellular matrix pro

261 ordings of cultured neonatal rat ventricular myofibroblasts revealed that TGF-beta1, applied for 24 t

262 We found that these cardiac myofibroblasts secrete milk fat globule-epidermal growth

263 -induced cardiac fibrosis in fibroblast- and myofibroblast-specific inducible Cre-expressing mouse li

264 ation, these cells transform to an activated myofibroblast state and play a fundamental role in myoca

265 Fibroblasts and myofibroblasts subsequently accumulate and deposit exces

266 fibrosis had increased numbers of MSLN+ aPFs/myofibroblasts, suggesting that MSLN may be a potential

267 novel clonal strain of rat cancer-associated myofibroblasts (TDFSM) was co-cultured with a pure rat c

268 nce of ligand counteracted TGF-beta-mediated myofibroblast terminal differentiation and collagen cont

269 rmore, we identified a population of cardiac myofibroblasts that appears in the heart after MI in hum

270 his disease is the accumulation of activated myofibroblasts that excessively deposit extracellular ma

271 essive production of extracellular matrix by myofibroblasts that often leads to cirrhosis and consequ

272 pha-smooth muscle actin (alpha-SMA)-positive myofibroblasts that produced ECM proteins, including col

273 broblast activation and differentiation into myofibroblasts that secrete extracellular matrix protein

274 brosis is caused by EMT-driven generation of myofibroblasts, the effector cells of fibrosis that prod

275 identify compounds that inactivate human HSC myofibroblasts through the quantification of lipid dropl

276 fness regulates the ability of fibrotic lung myofibroblasts to invade the basement membrane (BM).

277 ase was demonstrated to induce fibroblast-to-myofibroblast transdifferentiation by activation of p38

278 Fibroblasts proliferate, undergo myofibroblast transdifferentiation, and deposit large am

279 ant functional cardioprotection with reduced myofibroblast transformation and fibrosis.

280 in-C stimulates collagen gene expression and myofibroblast transformation via TLR4 signalling.

281 o fuse to keratocytes in vitro and to induce myofibroblast transformation.

282 o produce TGF-beta2, promoting fibroblast-to-myofibroblast transformation; Loxl2 also acts downstream

283 , prevented TGFbeta from inducing epithelial-myofibroblast transition and cell migration but did not

284 coactivator of serum response factor, drives myofibroblast transition from various precursors.

285 eriments suggest that Gbeta5 facilitates the myofibroblast transition, the persistence of which contr

286 Nox4 knockdown abrogates epithelial-myofibroblast transition-associated reactive oxygen spec

287 x state and impact epithelial plasticity and myofibroblast transition.

288 We found that myofibroblasts triggered cues in the tumor microenvironm

289 ha-smooth muscle actin expression by infarct myofibroblasts was not affected by Smad3 loss.

290 ctions of IL10KO chimeric mice suggests that myofibroblasts were derived from bone marrow after trans

291 henotypic switches of cardiac fibroblasts to myofibroblasts were observed.

292 In vivo, we found that TAM and myofibroblasts were the main sources of IGF production,

293 MSCs differentiate into myofibroblasts when RhoA/ROCK is turned on, endothelial

294 Radixin was also synthesized by the myofibroblasts, whereas ezrin colocalized with the myofi

295 In this study, we demonstrated that cardiac myofibroblasts, which execute tissue fibrosis by produci

296 ans-differentiation of quiescent HSCs to HSC myofibroblasts, which secrete extracellular matrix prote

297 is is the transformation of fibroblasts into myofibroblasts, which secrete large amounts of extracell

298 ulations of proliferating fibroblasts and of myofibroblasts, which were both reduced by FG-3019.

299 gene specifically in cardiac fibroblasts or myofibroblasts with 2 different tamoxifen-inducible Cre

300 Treatment of GLS1-deficient myofibroblasts with exogenous glutamate or alpha-KG rest