ライフサイエンスコーパス: fibrotic

1 phatic collecting vessels hyperpermeable and fibrotic.

2 these studies suggest a novel paradigm where fibrotic activation in MCs increases PI3K dependent mTOR

3 This work supports the notion that anti-fibrotic activities of ROCK-inhibitors could counteract

4 reased frequency, activation status and anti-fibrotic activity compared with those from chronic hepat

5 2 as a potential mediator of apigenin's anti-fibrotic activity.

6 top-ranked compounds predicted to have anti-fibrotic activity; indeed, apigenin dose-dependently red

7 facilitates discovery of novel pro- and anti-fibrotic agents in 384-well plate format and may be wide

8 inflammatory cells, cytokine signatures, and fibrotic airway remodeling.

9 Furthermore, there was a shift away from pro-fibrotic/alternative pro-fibrotic macrophage signaling a

10 We isolated 10 primary fibrotic and 7 non-fibrotic conjunctival fibroblast cell

11 of muscle fibers, and their substitution by fibrotic and adipose tissue.

12 that chronic necroptosis may underlie human fibrotic and autoimmune disorders.

13 Tumors are fibrotic and characterized by abundant, remodeled, and c

14 ed 21 genes differentially expressed between fibrotic and control lung tissue (Q < 0.001), many of wh

15 ericytes and glia largely segregate into the fibrotic and glial scars, respectively; therefore, we us

16 PDAC cells as an important regulator of the fibrotic and immunosuppressive TME.

17 hepatic expression of pro-inflammatory, pro-fibrotic and inflammasome genes.

18 s, with bleomycin-treated mice mimicking the fibrotic and inflammatory components of SSc and endothel

19 r immune cell infiltration and expression of fibrotic and inflammatory markers than kidneys of FA-tre

20 the poorly understood ECM composition of the fibrotic and tumor microenvironment is an underexplored

21 n relaxin-2) is a peptide molecule with anti-fibrotic and vasoprotective properties that binds to rel

22 TGF-alpha overexpression revealed a layered fibrotic appearance.

23 esin-positive cells were embedded within the fibrotic areas between the myofibers adjacent to the col

24 ithin mild fibrosis regions; while in severe fibrotic areas, they were either directly attached to or

25 tay of therapy for patients with predominant fibrotic atrial cardiomyopathy.

26 hMSC PS was also revealed in simulations of fibrotic cardiac tissue, where hMSC PS protected from po

27 otensin II induced extensive hypertrophy and fibrotic cardiomyopathy, with increased cardiac apoptosi

28 While macrophages are indispensable to the fibrotic cascade, surprisingly neutrophils and complemen

29 The PRG4 gene was also downregulated in fibrotic cell lines (0.002) compared with nonfibrotic ce

30 The IL6 gene was upregulated in fibrotic cell lines (mean, 0.040) compared with nonfibro

31 ated and 200 genes were downregulated in the fibrotic cell lines compared to the non-fibrotic cell li

32 the fibrotic cell lines compared to the non-fibrotic cell lines.

33 on on stiff culture substrates activates pro-fibrotic cell programs that are retained by mechanical m

34 entricular activation, correlating them with fibrotic change for the first time, adding activation ab

35 ein leads to lens degeneration, necrosis and fibrotic change, postnatally.

36 d following beta-agonist challenge, and upon fibrotic change.

37 ly thought to be the underlying cause of the fibrotic changes that underlie idiopathic pulmonary fibr

38 ethanol) stresses, long before more-dramatic fibrotic changes to the liver occur.

39 reverse the adverse effects that precipitate fibrotic changes, drusen formation, tractional retinal d

40 al cells (HK-2), TGF-beta1 treatment induced fibrotic changes, including collagen I and vimentin expr

41 ession levels and beta-catenin activation in fibrotic/cirrhotic human liver tissues.

42 F expression was reduced in tubular cells in fibrotic compared with healthy murine and human kidneys.

43 regulated in human alveolar macrophages from fibrotic compared with normal lungs.

44 decreased the expression of profibrotic and fibrotic components, including fibronectin, alpha-smooth

45 -JUN is a central molecular mediator of most fibrotic conditions.

46 ne model, whereas FIEL1 knockdown attenuates fibrotic conditions.

47 We isolated 10 primary fibrotic and 7 non-fibrotic conjunctival fibroblast cell lines from patient

48 s, matrix metalloproteinases (MMPs), and pro-fibrotic cytokine, TGF-beta1, and enzymes, tissue inhibi

49 increased CF release of inflammatory and pro-fibrotic cytokines and matrix metalloproteinases.

50 ibrosis and suppression of intracardiac anti-fibrotic cytokines, while premenopausal diabetic female

51 olymers in the airways and expression of pro-fibrotic cytokines.

52 cal translation for assessing and monitoring fibrotic damage.

53 mainly perivascular inflammatory infiltrate, fibrotic degeneration, and neovascularization after 6 ho

54 tory disease of the pancreas, leading to its fibrotic destruction.

55 Systemic sclerosis (SSc) is a spreading fibrotic disease affecting the skin and internal organs.

56 development and wound healing, and occurs in fibrotic disease and carcinoma.

57 critical driver of collagen accumulation and fibrotic disease but also a vital suppressor of inflamma

58 and MSC-like cells in myofibroblast-mediated fibrotic disease in the kidney, lung, heart, liver, skin

59 Fibrotic disease is associated with matrix deposition th

60 A hallmark of fibrotic disease is the excessive accumulation of extrac

61 en FSR correlates with established risks for fibrotic disease progression in NASH, and plasma lumican

62 ensing process in complex tissues, including fibrotic disease states with high collagen, is now utili

63 pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis.

64 clerosis (scleroderma, SSc) is a devastating fibrotic disease with few treatment options.

65 Systemic sclerosis (SSc) is a multi-organ fibrotic disease with few treatment options.

66 opathy, which correlates with progression of fibrotic disease.

67 fferences, it was assumed that the different fibrotic diseases also have different pathomechanisms.

68 Fibrotic diseases are not well-understood.

69 licated in aberrant fibroblast activation in fibrotic diseases including systemic sclerosis (SSc).

70 rocess of fibrosis, a deadly complication of fibrotic diseases like scleroderma (SSc).

71 ta promotes excessive collagen deposition in fibrotic diseases such as idiopathic pulmonary fibrosis

72 icated in several diseases including cancer, fibrotic diseases, and inflammation, among others.

73 s a potential therapy for cardiovascular and fibrotic diseases, but its short in vivo half-life is an

74 drome, lung adenocarcinoma, and debilitating fibrotic diseases, but the critical transcription factor

75 ic target for a number of diseases including fibrotic diseases, cancer, and inflammation, among other

76 Here, we demonstrate that many endstage fibrotic diseases, including IPF; scleroderma; myelofibr

77 present a novel opportunity to target deadly fibrotic diseases.

78 is a potential therapeutic strategy to treat fibrotic diseases.

79 neficial effects to block the progression of fibrotic diseases.

80 g from cardiovascular and renal disorders to fibrotic diseases.

81 cessive deposition of type I collagen causes fibrotic diseases.

82 tial therapeutic targets in the treatment of fibrotic diseases.

83 y fibrosis (IPF), which is a very aggressive fibrotic disorder.

84 mmation are epigenetically controlled in the fibrotic disorders involved in retinal detachment, but r

85 e structure and composition of wild-type and fibrotic ECM, we show that collagen in the ECM is organi

86 fibrotic Wnt/TGFbeta axis underlies its anti-fibrotic effect in aging, dystrophic muscle.

87 emains unclear whether FXR plays direct anti-fibrotic effect in renal fibrosis via regulating TGFbeta

88 in the progression of silicosis and the anti-fibrotic effect of Ac-SDKP.

89 o TGFbeta1 exposure and required for its pro-fibrotic effect.

90 erefore examined if CTGF inhibition has anti-fibrotic effects in PF.

91 nt fibroblasts are less sensitive to the pro-fibrotic effects of TGFbeta.

92 of SM, had strong anti-inflammatory and anti-fibrotic effects through its inhibition of inflammatory

93 sed from COL VI and promotes pleiotropic pro-fibrotic effects.

94 ard the central cornea underwent a transient fibrotic endothelial-mesenchymal transition (EMT) which

95 hypoxia- and chronic kidney disease-induced fibrotic events.

96 required in resident cardiac fibroblasts for fibrotic excessive extracellular matrix gene expression

97 ac fibroblasts is required for deposition of fibrotic extracellular matrix and the regulation of card

98 The fibrotic extracellular matrix remodeling is mediated by

99 einase-9 expressed in macrophages within the fibrotic extracellular matrix.

100 factor beta1 (TGFbeta1) is the principal pro-fibrotic factor, but its inhibition is associated with s

101 (TCAs), and they repressed expression of pro-fibrotic factors Alpha-Actin-2 (ACTA2) and Alpha-1 Type

102 yofibroblast accumulation, expression of pro-fibrotic factors, and accumulation of fibrotic tissue wi

103 MSCs, suggesting the presence of MSCs with a fibrotic fingerprint in papillary thyroid cancer tumors

104 organized clusters represents the origins of fibrotic foci after WTI and is promoted by a cross-talk

105 tructures, defining this region as an active fibrotic front.

106 e of TGF-beta significantly reversed NK anti-fibrotic function in vitro.

107 We analyzed frequency, phenotype and anti-fibrotic function of hepatic and peripheral NK subsets i

108 pathways: one enhances matrix deposition by fibrotic gene activation, whereas the other slows down m

109 GF-beta1/p38 MAPK signaling and induction of fibrotic gene expression in vivo.

110 TGF-beta1-induced SMAD3 phosphorylation and fibrotic gene expression, whereas PPM1A overexpression i

111 g in the downregulation of TGF-beta1-induced fibrotic gene expression.

112 gene promoter, leading to a decrease in the fibrotic gene expression.

113 constriction showed comparable increases in fibrotic gene expressions and ROS production but promote

114 downregulation of inflammatory cytokines and fibrotic gene expressions.

115 -induced H3K4me1 histone modification of the fibrotic gene promoter, leading to a decrease in the fib

116 ed expression of LV pro-inflammatory and pro-fibrotic genes and collagen deposition after MI compared

117 as well as the induction of inflammatory and fibrotic genes during chronic elevation of circulating T

118 RHR1 antagonist, inhibited the expression of fibrotic genes in vitro and decreased IBDM and hepatic f

119 crease in the expression of inflammatory and fibrotic genes including Emr1, Ccl2, Col1a1, Tgfb, Pdgfr

120 osis in vivo, inhibiting proinflammatory and fibrotic genes without affecting infection clearance.

121 mRNA levels of both pro-inflammatory and pro-fibrotic genes.

122 The fibrotic group had marked bleb scarring and vascularizat

123 ) had previously undergone glaucoma surgery (fibrotic group) (mean [SD] age, 43.8 [3.6 years]; 16 [57

124 umulate in CTS SSCT and that the presence of fibrotic growth factor, PDGF-AA, results in increased pr

125 ith PCOS contributes to the induction of pro-fibrotic growth factors during ovarian fibrosis, and tha

126 were found to increase the expression of pro-fibrotic growth factors, including transforming growth f

127 In the heart, acute injury induces a fibrotic healing response that generates collagen-rich s

128 ly important role in arrhythmogenesis of the fibrotic heart.

129 demonstrate that miR-125b is induced in both fibrotic human heart and murine models of cardiac fibros

130 GzmB was elevated in fibrotic human hearts and in angiotensin II-induced muri

131 otrophin derived during COL VI deposition in fibrotic human kidneys is a marker for progression of CK

132 o normal MCs (non-Fib MCs), MCs derived from fibrotic human lung allografts (Fib-MCs) demonstrated in

133 opathic pulmonary fibrosis (IPF) or chronic (fibrotic) hypersensitivity pneumonitis, which suggests t

134 Fibrotic idiopathic interstitial pneumonias (fIIP) are a

135 -gamma in a mouse model; however, their anti-fibrotic immune-characteristics and regulatory mechanism

136 r fat pad, a soft tissue that becomes highly fibrotic in the post-TKA joint, expresses multiple infla

137 Fibroblasts isolated from the post-TKA fibrotic infrapatellar fat pad express the IL-1 receptor

138 ltration, myofibroblast differentiation, and fibrotic injury both in prophylactic and early therapeut

139 in fibrosis and may play a role in promoting fibrotic injury.

140 protein 1 (YAP-1) are core mediators of pro-fibrotic integrin beta-1 signalling, with YAP-1 capable

141 Progressive fibrotic interstitial lung diseases (ILDs) are character

142 nhibited expression of pro-apoptotic and pro-fibrotic JNK and TGFbeta1 proteins in Ppif-/- females.

143 e discovered that many months after TKA, the fibrotic joint exists in a state of unresolved chronic i

144 ted for alleviating inflammation and pain in fibrotic joints and other tissues.

145 resulted in a relatively focal uptake in the fibrotic kidney and reduced renal fibrosis.

146 on as a therapeutic strategy in progressive, fibrotic kidney disease.

147 elopment of new treatments for patients with fibrotic kidney disease.

148 d to areas of increased COL VI deposition in fibrotic kidneys but was not present in histologically n

149 Notably, fibrotic kidneys had no evidence of inflammatory cytokin

150 nderlying the decreased response of REPCs in fibrotic kidneys to anemic stimulation remain elusive.

151 s of isoniazid in individuals with pulmonary fibrotic lesions and LTBI (n = 27830) found a reduction

152 In fibrotic lesions in human and mouse lungs, we found exte

153 non-invasive imaging of active cathepsins in fibrotic lesions of patients with IPF.

154 oth muscle actin (alpha-SMA) and collagen in fibrotic live tissues.

155 pheres released pPB-HSA into both plasma and fibrotic liver at 24 h after injection, which was mainta

156 Together, M2-like macrophages in fibrotic liver exert the protective effects against leth

157 were infused repeatedly into mice undergoing fibrotic liver injury.

158 In fibrotic liver tissue from mice and patients, hepatic S1

159 Hepatoprotection in the fibrotic liver was tightly related to innate immune tole

160 insult; conversely, depleting macrophages in fibrotic liver weakened the hepatoprotection and gave ri

161 pothesized that increased matrix rigidity in fibrotic livers would activate mechanotransduction in he

162 nalysis across liver lobules from normal and fibrotic livers.

163 Mesenchymal cells (MCs) derived from fibrotic lung allografts (BOS MCs) demonstrated constitu

164 +)/CD27(+)/CD45(-)/CD20(-) plasma B cells in fibrotic lung and skin tissue.

165 is (IPF) is a chronic, progressive and fatal fibrotic lung disease characterized by profound changes

166 Thus, our findings establish that fibrotic lung disease is mediated, in part, by senescent

167 is a prototype of chronic, progressive, and fibrotic lung disease.

168 group of acute and chronic inflammatory and fibrotic lung diseases.

169 anagement of patients with other progressive fibrotic lung diseases.

170 e IPF phenotype and regulate inflammation in fibrotic lung injury.

171 at matrix stiffness regulates the ability of fibrotic lung myofibroblasts to invade the basement memb

172 Fibrotic lung strips responded to tensile force by relea

173 intracellular distribution in fibroblasts on fibrotic lung, as compared with normal lung.

174 lar matrix (ECM) composition of normal lung, fibrotic lung, lung tumors, and metastases.

175 rusive activity in fibroblasts on normal and fibrotic lung.

176 obe (64)Cu-CBP7 showed the highest uptake in fibrotic lungs and the highest target-to-background rati

177 We reasoned that SIRT3 deficiency occurs in fibrotic lungs and thereby augments AEC mtDNA damage and

178 expression of miR-101 was down-regulated in fibrotic lungs from patients with IPF and bleomycin-trea

179 shift away from pro-fibrotic/alternative pro-fibrotic macrophage signaling after LVAD use.

180 Analysis of Masson trichrome staining and fibrotic marker protein and mRNA expression 14 days afte

181 ne the effect of VD supplementation on serum fibrotic markers in chronic hepatitis C (CHC) patients.

182 or alpha mRNA correlated with CCN2 and other fibrotic markers in the skin of SSc patients.

183 ation compared with changes in expression of fibrotic markers indicate the need to better understand

184 IHC, hydroxyproline content, and by qPCR for fibrotic markers.

185 attenuated TGF-beta-induced accumulation of fibrotic markers.

186 Desmoplasia, a fibrotic mass including cancer-associated fibroblasts (C

187 nuclear factor 4 alpha (HNF4alpha), whereas fibrotic matrix stiffness inhibited the HNF4alpha transc

188 uent Src activation in fibroblasts plated on fibrotic matrix, osteopontin.

189 increased ATX expression and activity in non-fibrotic MCs.

190 udy and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonar

191 acts as a potent repressor of multiple anti-fibrotic mechanisms.

192 Pro-fibrotic mesenchymal cells are known to be the key effec

193 RNAi-mediated gene silencing of il17a in fibrotic mice arrested the progression of lung fibrosis,

194 Macrophages in fibrotic mice exhibited M2-preponderant activation, whic

195 models, we found that myofibroblasts and the fibrotic microenvironment created by myofibroblasts impa

196 population, and may contribute to the stiff fibrotic microenvironment through their own stiffness bu

197 Our data suggest that miR-101 is an anti-fibrotic microRNA and a potential therapeutic target for

198 Downstream fibrotic molecules were upregulated.

199 molecules, Tenascin-C, and VEGF-A, while pro-fibrotic molecules, including several extracellular matr

200 GFbeta, reversed the increased expression of fibrotic molecules.

201 adult Id cDKO mice led to downregulation of fibrotic molecules.

202 hepatocyte-like cells from myofibroblasts in fibrotic mouse livers and reduced liver fibrosis.

203 Here, we generated a novel kidney fibrotic mouse model of persistent EGFR activation by se

204 get the structures and cells contributing to fibrotic muscle function.

205 Fibrotic muscles are stiffer and have a higher concentra

206 ute disease onset on cardiomyocyte death and fibrotic myocardial remodeling.

207 eported increased T cell infiltration in the fibrotic myocardium of nonischemic HF patients, as well

208 was reduced by TGFbeta antibody or the anti-fibrotic nintedanib.

209 hepatocellular carcinomas (HCCs) develop in fibrotic or cirrhotic livers, suggesting an important ro

210 44 expression have been detected in numerous fibrotic organs.

211 ere healing is deficient or compromised by a fibrotic outcome.

212 tory mediators, and in Wistar rats increased fibrotic overgrowth.

213 (PMF): prefibrotic/early (pre-PMF) and overt fibrotic (overt PMF) phase.

214 al microenvironment found within healthy and fibrotic pancreas, we demonstrate that matrix stiffness

215 c analyses indicate that early activation of fibrotic pathways in the kidney occurs before the onset

216 els reconstructed from clinical MRI scans of fibrotic patient atria to explore the feasibility of opt

217 CD31(+) vessels and VEGF-A-positive cells in fibrotic peritoneum.

218 tic mediators at >/=25 wk after irradiation (fibrotic phase).

219 During the fibrotic phase, monocyte-derived alveolar macrophages di

220 The fibrotic phenotype correlated with a reduction in the po

221 ty was also important for the development of fibrotic phenotype in conditional Vhlh knockout mice.

222 ty or downstream MEK activity attenuated the fibrotic phenotype.

223 the mechanistic pathways driving the complex fibrotic process in the eye and other tissues.

224 The fibrotic process is initiated by cytokines, neuroendocri

225 ) as prominent mediators of inflammatory and fibrotic processes during CP.

226 ssment of necroinflammatory, congestive, and fibrotic processes of chronic liver diseases.

227 thought that these cells stimulate and drive fibrotic progression.

228 esulting in more accurate staging throughout fibrotic progression.

229 A4 gain of function was sufficient to confer fibrotic properties to non-IPF MPCs.

230 g profile indicative of vasodilator and anti-fibrotic properties.

231 a chronic DSS model and impeded ex vivo pro-fibrotic protein secretion from stenotic CD biopsies.

232 nin and p-STAT3 were inversely correlated in fibrotic rat liver and HSC.

233 eripolesis in LC patients, providing an anti-fibrotic rational by enhancing NK cell activity.

234 Pancreatic cancer is accompanied by a fibrotic reaction that alters interactions between tumor

235 s expressing PW1(+) and their involvement in fibrotic remodeling after MI.

236 may also be an important determinant of pro-fibrotic remodeling during tissue fibrosis.

237 tion of macrophages and neutrophils, and (5) fibrotic remodeling of the airway wall.

238 ss and cross-clamp times are associated with fibrotic remodeling over a decade later.

239 onitored for survival, cardiac function, and fibrotic remodeling.

240 mineralocorticoid receptor (MR)-mediated pro-fibrotic remodeling.

241 iac contractility and a reduction in cardiac fibrotic remodeling.

242 HK2 protein and activity are up-regulated in fibrotic renal tissue.

243 eakdown, or loss of muscle, and accompanying fibrotic replacement.

244 kinase within the fibroblast to program the fibrotic response and myofibroblast formation in vivo, s

245 elastin and collagen expression, promoting a fibrotic response and subsequent stabilization of existi

246 rkedly reduced the pressure overload-induced fibrotic response as well as fibrosis mediated by a hear

247 The fibrotic response in Clusterin deficient (CLU-/-) mice p

248 and in vivo loss of Sox9 blunted the cardiac fibrotic response on ischemic injury.

249 ury incites an overwhelming inflammatory and fibrotic response that leads to expansive fibrous tissue

250 cient (Sphk2(-/-)) mice showed an attenuated fibrotic response to UUO compared with wild-type mice, a

251 ng adiponectin mounted an exaggerated dermal fibrotic response, while transgenic mice with constituti

252 ac fibroblasts as principal mediators of the fibrotic response.

253 rive myofibroblast formation and the cardiac fibrotic response.

254 k between inflammatory potential and initial fibrotic response.

255 thogenic leukocyte subtypes, which drive the fibrotic response.

256 IPF lung fibroblasts reduced the exacerbated fibrotic response.

257 ZYZ-168 appeared to inhibit the fibrotic responses in a concentration dependent manner,

258 ponectin receptor agonists abrogated ex vivo fibrotic responses in explanted normal and SSc fibroblas

259 In these rats, CRMS induces microvascular fibrotic responses in heart and kidneys, associated with

260 TLR4-, and C5aR-mediated proinflammatory and fibrotic responses to bacteria that were consistent with

261 l inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through down

262 f ROCK1 expectedly reduced TGF-beta1 induced fibrotic responses.

263 CI angiogenesis, which in turn is needed for fibrotic scar formation.

264 Predictive model of GA vs. fibrotic scar showed sensibility of 68.89% and specifici

265 Predictive model of preserved macula vs. GA/fibrotic scar showed sensibility of 77.78% and specifici

266 inal cord injury (SCI) induces a centralized fibrotic scar surrounded by a reactive glial scar at the

267 Fibroblasts persist within fibrotic scar tissue and exhibit considerable phenotypic

268 if this were also true in the CNS, then the fibrotic scar would depend on dividing NG2(+) pericytes.

269 on angiogenesis and completely abolished the fibrotic scar.

270 cellular matrix proteins responsible for the fibrotic scar.

271 mor sites, and two had just a small residual fibrotic scar.

272 pithelium detachment, and geographic atrophy/fibrotic scar/neovascular AMD in the fellow eye.

273 characterized by formation of astrocytic and fibrotic scars, both of which are necessary for lesion r

274 collecting lymphatic vessels were located in fibrotic septa between the exocrine lobules and adjacent

275 s on transforming growth factor-beta-induced fibrotic signaling in BM-FPCs.

276 We further evaluated fibrotic signaling in isolated murine primary ventricula

277 factor-beta-induced transdifferentiation and fibrotic signaling in WT BM-FPCs in vitro.

278 ass, extracellular matrix deposition and pro-fibrotic signaling, and also prevented mucus accumulatio

279 pression, MR activation, and MR-mediated pro-fibrotic signaling.

280 ove our understanding of the organization of fibrotic skeletal muscle extracellular matrix and identi

281 y donor control samples (n = 10), as well as fibrotic skin lesions from localized scleroderma and uni

282 ediate acute pneumonitis phase and the later fibrotic stage.

283 cies in response to a range of important pro-fibrotic stimuli.

284 tion assays: TGFbeta1 delivered a potent pro-fibrotic stimulus, which was reduced by TGFbeta antibody

285 are key mediators in the production of this fibrotic stroma, upon activation transitioning to a myof

286 Interestingly, treated tumors were more fibrotic than the control group.

287 ed a computational approach to identify anti-fibrotic therapies by querying a transcriptome.

288 Identification of molecular targets and anti-fibrotic therapies could provide new treatment strategie

289 ay be used as sensitive biomarkers to detect fibrotic tissue deposition and fiber atrophy in dystroph

290 nced carrier and payload accumulation in the fibrotic tissue facilitated sequence-specific gene knock

291 To this end, after 4 weeks of reperfusion, fibrotic tissue increased and myocardial strain echocard

292 plete senescent cholangiocytes and ASFs from fibrotic tissue to ameliorate liver fibrosis.

293 of pro-fibrotic factors, and accumulation of fibrotic tissue without affecting clinical disease activ

294 tinal tract and is activated in inflamed and fibrotic tissue.

295 sis, and LOXL2 is known to be upregulated in fibrotic tissue.

296 d confirmed the preferential accumulation in fibrotic tissue.

297 , embryonically derived TAMs exhibited a pro-fibrotic transcriptional profile, indicative of their ro

298 mising strategy for developing targeted anti-fibrotic treatments.

299 Fibrotic tumors contain abundant FN, and tumor cells fre

300 he wound can become chronic or progressively fibrotic, with both outcomes impairing tissue function,