ライフサイエンスコーパス: myofibroblast

1 ngle-lineage HSC trajectory from pericyte to myofibroblast.

2 f all fibrotic conditions is the activity of myofibroblasts.

3 into migratory extracellularmatrix-producing myofibroblasts.

4 nclear how aging increases the generation of myofibroblasts.

5 the number of OASIS-expressing pathological myofibroblasts.

6 and can be used as a cell surface marker of myofibroblasts.

7 re chemically and electrically influenced by myofibroblasts.

8 and transdifferentiation of hyalocytes into myofibroblasts.

9 ants of lung fibroblast differentiation into myofibroblasts.

10 phage recruitment, and increased presence of myofibroblasts.

11 e-cell RNA-sequencing on genetically labeled myofibroblasts.

12 cytes regulates the differentiation state of myofibroblasts.

13 g to the edge dynamics (lamellipodia) of the myofibroblasts.

14 in fibrogenesis in adult rat fibroblasts and myofibroblasts.

15 ly enlarged despite the normal appearance of myofibroblasts.

16 r transition of human cardiac fibroblasts to myofibroblasts.

17 s, including resting CFs, activated CFs, and myofibroblasts.

18 (transforming growth factor-beta)-activated myofibroblasts.

19 ifferentiation and survival of ECM-producing myofibroblasts.

20 t2) expression was reduced in OASIS knockout myofibroblasts.

21 ng and cancer that is commonly attributed to myofibroblasts.

22 ation of fibroblasts, and differentiation of myofibroblasts.

23 SULF1 is highly enriched in human and mouse myofibroblasts.

24 collagen and that predominantly laid-down by myofibroblasts.

25 urring in extracellular proteins secreted by myofibroblasts.

26 ls activated and transduced fibroblasts into myofibroblasts.

27 ape changes of type I cells and migration of myofibroblasts.

28 ed for TGFbeta-dependent Igf-1 expression in myofibroblasts; (4) demonstrates IGF-1R activation is es

29 he absence of smooth muscle actin-expressing myofibroblasts, a key profibrotic cell population.

30 Adipocytes regenerate from myofibroblasts, a specialized contractile wound fibrobla

31 1 24 hours post-RT had significantly reduced myofibroblast accumulation and collagen deposition 15 we

32 Excessive myofibroblast accumulation and persistence, often as a r

33 l cell phenotypes, which are associated with myofibroblast accumulation in the lung.

34 diated knockdown of SULF1 attenuates cardiac myofibroblast activation and collagen deposition.

35 xpression of SULF1 promotes TGF-beta-induced myofibroblast activation and partially antagonizes anti-

36 cological targeting of REVERBalpha inhibited myofibroblast activation in IPF fibroblasts and collagen

37 ed and important role for PA200 in adjusting myofibroblast activation in response to pro-fibrotic sti

38 uman ADPKD cystic epithelial cells increased myofibroblast activation in vitro, suggesting a paracrin

39 r the initial healing response but excessive myofibroblast activation leads to pathological fibrosis.

40 meostasis) and protect against inflammation, myofibroblast activation, and kidney functional decline.

41 es of human ADPKD cystic epithelial cells on myofibroblast activation.

42 l-adhesion formation, resulting in increased myofibroblast activation.

43 downstream effector of TGF-beta-induced lung myofibroblast activation.

44 n when administered to animals subsequent to myofibroblast activation.

45 onstrated alphaSma expression (indicative of myofibroblast activity), increased hyaluronan deposition

46 l VI) as a prominent downstream regulator of myofibroblast activity.

47 e 1 receptor (AT(1)R), which is expressed on myofibroblasts along with RXFP1 and AT(2)R, is unknown.

48 tally and is thought to require the alveolar myofibroblast (AMF).

49 tically, S100a4 haploinsufficiency decreases myofibroblast and macrophage content at the site of inju

50 ed along with higher collagen deposition and myofibroblasts and decreased expressions of MMP-1.

51 It is characterized by the emergence of myofibroblasts and early activation of pro-fibrotic sign

52 Alveolar epithelial cells, myofibroblasts and endothelial cells undergo coordinated

53 rmal alpha3-knockout mice exhibit more wound myofibroblasts and fewer cyclooxygenase 2 (Cox-2)-positi

54 epithelial cells can stimulate interstitial myofibroblasts and fibrosis in ADPKD kidneys.

55 nts the upregulation of IGF-1 via TGFbeta in myofibroblasts and fibrotic lung tissue, as well as its

56 They stimulate expansion of myofibroblasts and immune cells, followed by aggressive

57 entiation into cells that express markers of myofibroblasts and inflammatory chemokines and cytokines

58 Extensive immunohistochemical staining for myofibroblasts and procollagen III was observed in the n

59 cholangiocyte-derived signals that activate myofibroblasts and promote fibrosis.

60 ferentiation of cardiac fibroblasts (CFs) to myofibroblasts and promotes CF proliferation and fibrosi

61 ietic lineage cells give rise to a subset of myofibroblasts and rare regenerated adipocytes.

62 Growing evidence suggests that myofibroblasts and senescent myofibroblasts, rather than

63 tion of fibroblasts into apoptosis-resistant myofibroblasts and sustaining the production of extracel

64 into two states: the first with features of myofibroblasts and the second characterised by high expr

65 origins and differentiation of human kidney myofibroblasts and their precursors at high resolution.

66 differentiation contributes to expansion of myofibroblasts and to disease progression.

67 ition promotes activation of fibrotic cells (myofibroblasts) and impact tumors in a mutation-dependen

68 lation of alpha-smooth muscle actin-positive myofibroblasts, and bone marrow-derived fibrocytes.

69 lular matrix proteins, activation of hepatic myofibroblasts, and histological fibrosis.

70 agen deposition is exclusively attributed to myofibroblasts, and implicate macrophages as direct cont

71 identified two distinct expression patterns (myofibroblast- and fibroblast-like) from cells located i

72 While the origins of these myofibroblast appear to be diverse, fibroblast different

73 eases of myofibroblasts in aged organs where myofibroblasts are constantly generated from resident ti

74 In the cornea, myofibroblasts are derived primarily from stromal kerato

75 Myofibroblasts are fibroblast-like cells that secrete hi

76 Myofibroblasts are fibroblastic cells that function in w

77 cellular contacts between cardiomyocytes and myofibroblasts are highly dynamic, mainly owing to the e

78 Myofibroblasts are key contributors to pathological fibr

79 The protective actions of the myofibroblasts are mediated, at least in part, through S

80 Myofibroblasts are scar-forming cells that are ultimatel

81 Myofibroblasts are the key effector cells responsible fo

82 ivated, extracellular matrix (ECM)-producing myofibroblasts at sites of tissue injury is critical for

83 r cellular component (especially fibroblasts/myofibroblasts; average value range 69-150 cells/mm(2),

84 demonstrated defective differentiation into myofibroblasts but normal migration and F-actin content,

85 c stellate cells (HSCs) into tumor-promoting myofibroblasts but underlying mechanisms remain incomple

86 KPs deleted for Ccn2, differentiation into a myofibroblast, but not an adipocyte or neuronal phenotyp

87 hepatic stellate cells and stellate-derived myofibroblasts, but not in hepatocytes.

88 for new therapies that trigger apoptosis in myofibroblasts by blocking pro-survival mechanisms, targ

89 ew Zealand white rabbits and confirmed to be myofibroblasts by immunocytochemistry.

90 rentiation of dermal progenitor cells into a myofibroblast/CAF phenotype and is, therefore, a therape

91 g-standing debate regarding the existence of myofibroblast-cardiomyocyte electrical coupling in vivo.

92 cupancy revealed that Yap directly activates myofibroblast cell identity genes, the proto-oncogene My

93 2 mutant CFs spontaneously transitioned to a myofibroblast cell state.

94 last contractility, myofibroblast migration, myofibroblast collagen/fibronectin deposition, as well a

95 Cardiomyocyte-myofibroblast contact dynamism is modulated by connexin-

96 data show that heterocellular cardiomyocyte-myofibroblast contacts exhibit high dynamism.

97 PK via NFKB1 deletion enhance macrophage and myofibroblast content at the repair, driving increased c

98 decrease in profibrotic functions, including myofibroblast contractile force, extracellular matrix (E

99 cytostasis, mesenchymal differentiation, and myofibroblast contractility, in which NUAK1 or NUAK2 sil

100 including myosin light-chain kinase-mediated myofibroblast contractility, myofibroblast migration, my

101 iptional mechanisms underlying fibroblast-to-myofibroblast conversion in the heart have not been expl

102 This finding indicated that fibroblast-to-myofibroblast conversion is mechanistically coupled to c

103 tic program in cardiac fibroblasts, inducing myofibroblast conversion, and stimulating synthesis of b

104 ly increased blood vessel density, decreased myofibroblast density and collagen content, augmented ca

105 econstruction, we found that Hippo-deficient myofibroblasts deployed a network of transcriptional reg

106 nist, for 3 days and evaluated the effect on myofibroblast deposition of extracellular matrix (ECM).

107 n senescent human mesenchymal stem cells and myofibroblasts derived from patients with Hutchinson-Gil

108 ssue stiffening contribute to fibroblast and myofibroblast differentiation and activation, which furt

109 betaR signaling does not significantly alter myofibroblast differentiation and collagen secretion wit

110 ificantly attenuated collagen deposition and myofibroblast differentiation and expansion in UUO and a

111 gnaling pathway in the control of fibroblast-myofibroblast differentiation and fibrosing lung injury.

112 anges of collagen microarchitecture regulate myofibroblast differentiation and fibrosis independent o

113 (2+)) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis.

114 Myofibroblast differentiation is accompanied by changes

115 Fibroblast to myofibroblast differentiation is crucial for the initial

116 lar collagen networks mechanically regulates myofibroblast differentiation of adipose stromal cells (

117 t PA200 functions as a negative regulator of myofibroblast differentiation of human but not mouse cel

118 Here, we show that myofibroblast differentiation of mural cells contributes

119 Specific inhibition of proliferation and myofibroblast differentiation of primary, murine cardiac

120 on of mechanotransduction pathways prevented myofibroblast differentiation of SKPs and expression of

121 tension sensation at focal adhesions induced myofibroblast differentiation on aligned mimetics.

122 ng growth factor beta 1-driven fibroblast-to-myofibroblast differentiation promotes HYAL2 cytoplasmic

123 GFbetaR attenuates Myh11+ retinal mural cell myofibroblast differentiation, and diminishes the subseq

124 MAP3K19 was required for IPF myofibroblast differentiation, and targeting its activit

125 Alignment cues also induced myofibroblast differentiation, as >60% of fibroblasts fo

126 Consistent with elevated myofibroblast differentiation, ASCs in scaffolds with th

127 Targeting activated fibroblasts, including myofibroblast differentiation, has emerged as a key ther

128 2) disrupts TGFbeta signaling and suppresses myofibroblast differentiation, however practical strateg

129 and metabolic mechanisms that contribute to myofibroblast differentiation, persistence, and function

130 shown to influence mRNA splicing to prevent myofibroblast differentiation.

131 associate domain) binding were required for myofibroblast differentiation.

132 derived mesenchymal stem cells, with ensuing myofibroblast differentiation.

133 mbin, plasmin and uPA all induced fibroblast/myofibroblast differentiation.

134 d Col-1 and reduced morphological changes of myofibroblast differentiation.

135 enhanced collagen production in response to myofibroblast differentiation.

136 ich effect collagen microarchitecture has on myofibroblast differentiation.

137 Myofibroblasts drive fibrosis, thereby promoting progres

138 Excessive collagen deposition by myofibroblasts during adverse cardiac remodeling leads t

139 as the main cellular sources of scar-forming myofibroblasts during human kidney fibrosis.

140 stellate cells (HSCs) as they transition to myofibroblasts during liver injury and the wound healing

141 ls (MSCs), previously shown to contribute to myofibroblasts during scarring, promote metaplastic diff

142 Myofibroblasts evade apoptosis by activating molecular m

143 In developing fibrosis, myofibroblasts exist along an activation continuum of ph

144 l inflammation-coupled airway remodeling and myofibroblast expansion in the mouse model of aeroallerg

145 prevents epithelial mesenchymal transition, myofibroblast expansion, IgE sensitization, and fibrosis

146 ic YAP and YAP/TAZ knockouts exhibit limited myofibroblast expansion, less inflammation, and decrease

147 we also demonstrated that renal and cardiac myofibroblasts expressed all three receptors and that an

148 act with other essential cell types, such as myofibroblasts/fibroblasts, remain unclear.

149 ng pro-survival mechanisms, target senescent myofibroblast for apoptosis or promote the reprogramming

150 is required in alveolar epithelial cells and myofibroblasts for alveologenesis in mammals.

151 We studied mice silenced exclusively in myofibroblasts for PC1 and evaluated the role of PC1 in

152 m that are necessary to initiate and sustain myofibroblast formation and function.

153 n the mutant is further explained by reduced myofibroblast formation and upregulation of components o

154 Although myofibroblast formation is a physiological response to a

155 broblasts from radiation-induced cell death, myofibroblast formation, and senescence.

156 tive to understand the mechanisms underlying myofibroblast formation.

157 thods: ER expression in male lung tissue and myofibroblasts from control subjects (n = 6) and patient

158 ding the remodeling phase, and tenocytes and myofibroblasts from the Scleraxis (Scx) lineage were the

159 el therapeutic strategy for interfering with myofibroblast function in fibrosis and potentially in ot

160 ways that are important for full profibrotic myofibroblast functionality.

161 ential to support TGFbeta-driven profibrotic myofibroblast functions and excessive wound healing; and

162 am RhoA signaling and influences profibrotic myofibroblast functions, including myosin light-chain ki

163 ibroblasts in an activated state and control myofibroblast functions.

164 omatin accessibility in loci specific to the myofibroblast gene program, resulting in differentiation

165 ploinsufficiency is sufficient for enhancing myofibroblast generation, leading to multiorgan fibrosis

166 Hyalocytes, contractile myofibroblasts, glial cells, matrix metalloproteinases-2

167 P-TEAD signaling, which likely contribute to myofibroblast heterogeneity in the infarcted myocardium.

168 insights regarding the mechanistic basis for myofibroblast heterogeneity in the injured heart.

169 ted strong expression of TRPA1 in human lung myofibroblasts, human airway smooth muscle cells but not

170 In fibroblasts and myofibroblasts, HYAL2 interacts with the GTPase-signalin

171 lation in renal tubular epithelial cells and myofibroblasts in a murine model of unilateral ureteral

172 udies have identified many-fold increases of myofibroblasts in aged organs where myofibroblasts are c

173 ur understanding of the mechanisms that keep myofibroblasts in an activated state and control myofibr

174 which spontaneously transdifferentiate into myofibroblasts in culture.

175 One source of myofibroblasts in fibrosis is an endothelial-to-mesenchy

176 hypothesized that the persistent activity of myofibroblasts in fibrotic diseases might involve epigen

177 Consistent with this, myofibroblasts in human tendon scar samples displayed en

178 confirmed persistent NF-kappaB activation in myofibroblasts in human tendon scar tissue.

179 ivation blocks the dDAVP-induced increase in myofibroblasts in Pkd1KO kidneys.

180 f CCN2 significantly reduced cyst growth and myofibroblasts in Pkd1KO mouse kidneys.

181 ardiac fibroblasts, which differentiate into myofibroblasts in response to injury or stress.

182 transition of fibroblasts toward profibrotic myofibroblasts in response to transforming growth factor

183 s efficiently targeted endothelial cells and myofibroblasts in the alveolar region.

184 ss that includes a decrease in the number of myofibroblasts in the interstitium and degradation of th

185 ation of bone marrow-derived fibroblasts and myofibroblasts in the kidney following treatment with DO

186 ithelial cell apoptosis and proliferation of myofibroblasts in the lungs.

187 fferentiation of adipocytes (fat cells) into myofibroblasts in the pathogenesis of dermal fibrosis.

188 m by which cystic epithelial cells stimulate myofibroblasts in the pericystic microenvironment, leadi

189 -alpha were isolated and differentiated into myofibroblasts in the presence of Ang II (angiotensin II

190 ardiac fibroblasts from differentiating into myofibroblasts in the presence of TGFbeta when tested in

191 the protective effects of activated cardiac myofibroblasts in the pressure-overloaded myocardium are

192 plied to primary rat renal and human cardiac myofibroblasts in vitro, and in three models of renal- o

193 n SM alpha-actin and fibrogenesis in hepatic myofibroblasts in vivo.

194 key pathogenic cells in liver fibrosis, i.e. myofibroblasts including activated HSCs that highly expr

195 Conversely, 4PB-treated myofibroblasts increased their functional coupling to ca

196 Furthermore, adipocyte mediated myofibroblast induction occurred through a TGF-beta inde

197 Thereafter, we inject the engineered myofibroblasts into heart tissues and show their ability

198 or apoptosis or promote the reprogramming of myofibroblasts into scar-resolving cells.

199 of EndMT in vivo and reported 27% to 35% of myofibroblasts involved in cardiac fibrosis and 16% of i

200 ion of pancreatic stellate cells (PSCs) into myofibroblasts is inhibited by the estrogen-receptor mod

201 derlying collagen gene expression in cardiac myofibroblasts is therefore an important clinical goal.

202 of patient-derived intestinal subepithelial myofibroblasts (ISEMFs) and endothelial cells (ECs) into

203 ri stimulates increased secretion of Rspo by myofibroblasts, leading to an increase in proliferation

204 of Lgr5(+) cells or the knockout of Rspo3 in myofibroblasts leads to hypercolonization of the gastric

205 ment, being characterized by the presence of myofibroblast-like cancer-associated fibroblasts (CAFs).

206 as an option for mechanical reprogramming of myofibroblast-like cells in the tumour microenvironment.

207 Nkx2.3 expression was restricted to VAP-1(+) myofibroblast-like pericryptal cells.

208 her levels of MARCKS phosphorylation and the myofibroblast marker alpha-smooth muscle actin (alpha-SM

209 onally, trametinib reduced the expression of myofibroblast marker alpha-smooth muscle actin and the p

210 macrophage-associated genes (Adgre1, Ccl2), myofibroblast markers (Acta2), and general inflammation

211 cker fibers were more contractile, expressed myofibroblast markers, and deposited more extended fibro

212 se activity, and prevented the expression of myofibroblast markers.

213 inhibitor 9-ING-41 blocked the induction of myofibroblast markers; alpha-SMA and Col-1 and reduced m

214 Our results suggest BM-derived myofibroblasts may be more prone to the formation of exc

215 interactions between the three receptors on myofibroblasts may represent new targets for controlling

216 egulated differentiation of fibroblasts into myofibroblasts (MF) is critical for skin wound healing.

217 a-smooth muscle actin (alpha-SMA) expressing myofibroblasts (MFBs) with increased capacity to synthes

218 and OASIS contributed to TGF-beta1-mediated myofibroblast migration and increased proliferation.

219 biologic processes, including fibroblast and myofibroblast migration and proliferation, inflammation,

220 kinase-mediated myofibroblast contractility, myofibroblast migration, myofibroblast collagen/fibronec

221 circular morphology similar to the disparate myofibroblast morphologies measured in vivo.

222 ly decreased the number of cancer-associated myofibroblasts (myCAF).

223 tion and differentiation of fibroblasts into myofibroblasts (MyoFb).

224 asured by using histology, collagen content, myofibroblast numbers, and selected reaction monitoring.

225 lls over mucus-producing cells and decreased myofibroblast numbers, even in the context of continuous

226 upregulated in hyperplastic basal cells and myofibroblasts of fibrotic lungs from patients with idio

227 idney in vivo and in activated primary human myofibroblasts of the lung in vitro.

228 Here, we seeded myofibroblasts on substrates micropatterned with stripes

229 e therapy capable of selectively eradicating myofibroblasts or limiting their genesis.

230 pha expression increased in IPF lung tissue, myofibroblasts, or BLM mice.

231 acute injury, such as myocardial infarction, myofibroblast persistence, as occurs in heart failure, c

232 ced Gli1(+) PMCs proliferated and acquired a myofibroblast phenotype after cholestatic injury; Gli1(+

233 successfully identified genes affecting the myofibroblast phenotype of SSc skin fibroblasts.

234 dgehog signaling that proliferate, acquire a myofibroblast phenotype, and surround the biliary tree i

235 nto a highly contractile, collagen producing myofibroblast phenotype.

236 a paracrine factor that regulates the wound myofibroblast phenotype.

237 ced transcription of genes associated with a myofibroblast phenotype.

238 using dDAVP increased the renal interstitial myofibroblast population and ECM deposition.

239 oduction, and expansion of the subepithelial myofibroblast population.

240 roblasts and primary hepatic stellate cells (myofibroblast precursors in the liver) in vitro, and IL-

241 red cornea-derived and BM-derived alpha-SMA+ myofibroblast primary cultures were generated from four

242 Myofibroblasts produce desmoplastic stroma around tumors

243 ntion of aberrant cardiomyocyte coupling and myofibroblast proliferation in the infarct border zone.

244 nd decreasing both collagen accumulation and myofibroblast proliferation.

245 ic knockout of OASIS, accompanied by reduced myofibroblast proliferation.

246 activation, which entails differentiation to myofibroblasts, proliferation, migration, and collagen d

247 Taken together, OASIS in myofibroblasts promotes kidney fibrosis, at least in par

248 of SNAIL and fibrogenic factors stimulating myofibroblasts, promoting intratumoral fibrosis and supp

249 e suggests that myofibroblasts and senescent myofibroblasts, rather than being resistant to apoptosis

250 ment with let-7 mimic transfections in human myofibroblasts reduced ERalpha expression and associated

251 In vitro, the myofibroblast response as measured by Acta2 mRNA express

252 ing macrophage survival and by promoting the myofibroblast response.

253 The precise source of the myofibroblasts responsible for matrix deposition is not

254 Finally, myofibroblast-restricted OASIS conditional knockouts res

255 -associated transformation of fibroblasts to myofibroblasts, resulting in tissue fibrosis.

256 ivated Pdgfra postnatally in secondary crest myofibroblasts (SCMF), a subpopulation of lung mesenchym

257 ells with low Wnt activity were increased by myofibroblast-secreted factors, including HGF.

258 Tumorigenicity, however, was increased with myofibroblast-secreted factors, which was in the same di

259 tivation and proliferation of fibroblasts to myofibroblasts, secretion and accumulation of extracellu

260 n phenotype toward a mesenchymal cell (e.g., myofibroblast, smooth muscle cell).

261 F-1) are known to promote fibrosis; however, myofibroblast specific upregulation of IGF-1 in the init

262 broblasts to cardiomyocytes is reduced after myofibroblast-specific Cx43 down-regulation.

263 growth factor beta), additively upregulated myofibroblast-specific ECM genes independent of topograp

264 th muscle actin) stress fibers and expressed myofibroblast-specific ECM genes like Postn (periostin).

265 o express alphaSMA albeit with downregulated myofibroblast-specific ECM genes.

266 herapeutic targets, and identified NKD2 as a myofibroblast-specific target in human kidney fibrosis.

267 Paired cornea- and BM-derived myofibroblast specimens from each rabbit were analyzed b

268 results in a spontaneous transition toward a myofibroblast state that underlies fibrosis and ventricu

269 y reducing the frequency and activity of the myofibroblast subset, while promoting the formation of a

270 ct from the pro-fibrotic alphaSMA-expressing myofibroblast subtype.

271 We also uncovered novel myofibroblast subtypes expressing either pro-fibrotic or

272 ersistent NF-kappaB signaling may facilitate myofibroblast survival and fibrotic progression.

273 ogenitor-dependent functional differences in myofibroblasts that could impact tissue development.

274 tifies a novel HYAL2 cytoplasmic function in myofibroblasts that is unrelated to its enzymatic activi

275 revents the transformation of fibroblasts to myofibroblasts, the effect on alveolar type 2 (AT2) epit

276 hiregulin induced their differentiation into myofibroblasts, thereby selectively contributing to the

277 modulation is critical for the generation of myofibroblasts through endothelial-mesenchymal transitio

278 cient fibroblasts transform spontaneously to myofibroblasts through hyperactivation of transforming g

279 Intercellular calcein transfer from myofibroblasts to cardiomyocytes is reduced after myofib

280 inal microvasculature and differentiate into myofibroblasts to form an epiretinal membrane.

281 Cells), HSCs (Hepatic Stellate Cells) and/or myofibroblasts to mimic in vivo fibrotic responses and d

282 However, the mechanisms that help myofibroblasts to persist in fibrotic tissues remain poo

283 anilloid 4 (TRPV4) is a critical mediator of myofibroblast transdifferentiation and in vivo fibrosis

284 t both TRPV4 and PI3Kgamma were required for myofibroblast transdifferentiation as assessed by the in

285 specific therapeutic approach for inhibiting myofibroblast transdifferentiation.

286 s to the plasma membrane, thereby increasing myofibroblast transdifferentiation.

287 nduced TRPV4 plasma membrane recruitment and myofibroblast transdifferentiation.

288 ly observed, can arise through macrophage-to-myofibroblast transformation (MMT).

289 SIS expression coincident with fibroblast-to-myofibroblast transition and OASIS contributed to TGF-be

290 tory networks that control the fibroblast-to-myofibroblast transition.

291 ich inhibited Rho activation associated with myofibroblast transition.

292 wth factor-beta1 (TGF-beta1)-activated human myofibroblasts underwent multimerization by o,o'-dityros

293 Smad3 loss in activated periostin-expressing myofibroblasts using a mouse model of cardiac pressure o

294 ature alpha-smooth muscle actin (alpha-SMA)+ myofibroblasts (verified by immunocytochemistry for vime

295 er, S100a4-lineage cells become alpha-SMA(+) myofibroblasts, via loss of S100a4 expression.

296 However, the increased staining for myofibroblasts was not statistically significant in TCP-

297 aced by podocytes and supported by mesangial myofibroblasts, which ensure plasma filtration at the po

298 Specifically, we hybridize cardiac myofibroblasts with silicon nanowires and use these engi

299 cruitment and expansion of cancer-associated myofibroblasts within cholangiocarcinoma (CCA) stroma as

300 alter their fate and generate ECM-producing myofibroblasts within wounds.