ライフサイエンスコーパス: fibrosis

1 or-beta1 (TGF-beta1) plays a premier role in fibrosis.

2 ch are important in the progression of liver fibrosis.

3 inflammation, impaired microcirculation, and fibrosis.

4 idence of more severe graft inflammation and fibrosis.

5 nter reactions and resulting in target organ fibrosis.

6 broproliferative phase, leading to pulmonary fibrosis.

7 ing persistence of the transitional state in fibrosis.

8 liver enzymes, hepatic steatosis and hepatic fibrosis.

9 thus may have an important role in limiting fibrosis.

10 el during renal injury and the resolution of fibrosis.

11 ed challenges, and their utility in reducing fibrosis.

12 to treat different models of lung injury and fibrosis.

13 ifferentiation, and development of pulmonary fibrosis.

14 ion, an event that induces kidney injury and fibrosis.

15 reduce liver fat content or markers of liver fibrosis.

16 airway and alveolar epithelium in regions of fibrosis.

17 also arthritis, heart diseases, or pulmonary fibrosis.

18 steatohepatitis (NASH) and significant liver fibrosis.

19 helial niche S1PR1 to spur regeneration over fibrosis.

20 he location and severity of inflammation and fibrosis.

21 ge, a period representing the progression of fibrosis.

22 ling could be leading to cachexia-associated fibrosis.

23 ling, but can go awry, as in oncogenesis and fibrosis.

24 ortal hypertension and in experimental mouse fibrosis.

25 efined patients with risk for advanced liver fibrosis.

26 mited means to effectively reduce or reverse fibrosis.

27 ral and polar lipids, grade of steatosis and fibrosis.

28 bitors attenuate bleomycin-induced pulmonary fibrosis.

29 tions were grossly identified based on focal fibrosis.

30 ker, to treat liver adenocarcinoma and liver fibrosis.

31 its mucolytic action in patients with cystic fibrosis.

32 res features with mammalian wound healing or fibrosis.

33 heart regeneration, accompanied by decreased fibrosis.

34 pair, persistent inflammation contributes to fibrosis.

35 r niche to determine regenerative outcome in fibrosis.

36 njury results in devastating skeletal muscle fibrosis.

37 several diseases, including some cancers and fibrosis.

38 rchestrates leukocyte infiltration and organ fibrosis.

39 e host-pathogen interactions exist in cystic fibrosis.

40 ymal cells to promote liver inflammation and fibrosis.

41 ion implicated in murine models of pulmonary fibrosis.

42 er fibrosis, and 20 with mild-moderate liver fibrosis.

43 rkers in older mice, lipid peroxidation, and fibrosis.

44 presenting with pulmonary infiltrates and/or fibrosis.

45 library screens for the treatment of cardiac fibrosis.

46 ne expression of markers of inflammation and fibrosis.

47 B-839 attenuated bleomycin-induced pulmonary fibrosis.

48 onounced in persons with more advanced liver fibrosis.

49 he expression of mRNA and protein markers of fibrosis.

50 lying diseases including HIV/AIDS and cystic fibrosis.

51 ions for a cure for all patients with cystic fibrosis.

52 les in allergic diseases, asthma, and tissue fibrosis.

53 deposits, tubular injury, inflammation, and fibrosis.

54 dothelial cells are an integral part in lung fibrosis.

55 factor JUN is highly expressed in pulmonary fibrosis.

56 ion and the subsequent development of kidney fibrosis.

57 odelling of extracellular matrix proteins in fibrosis.

58 n of glutaminase 1 (GLS1) reverses pulmonary fibrosis.

59 and of mice upon bleomycin-induced pulmonary fibrosis.

60 therapeutic approach for treatment of renal fibrosis.

61 ed in the bleomycin mouse model of pulmonary fibrosis.

62 ression from the initial lesion to the final fibrosis.

63 vanced compared with earlier stages of liver fibrosis.

64 atic parenchyma and promote inflammation and fibrosis.

65 chanisms of HE4 in the pathogenesis of renal fibrosis.

66 a measure (L(f) ) was used to quantify liver fibrosis.

67 ITs in F3 and for ELF, NAFLD Fibrosis Score, Fibrosis-4 (FIB-4), and liver stiffness in F4).

68 x/+); Postn(MCM/+)) strongly reduces cardiac fibrosis (~50% reduction) in isoproterenol-, transverse

69 CFTR mutations cause cystic fibrosis, a lethal incurable disease.

70 h3 receptors on resident cells blunts kidney fibrosis, ablates NF-kappaB signaling, and lessens matri

71 he presence of NASH and concomitant advanced fibrosis (AF) was significantly associated with clinical

72 Mice with liver fibrosis after BDL had increased hepatic PFKFB3; injecti

73 a significant albeit transient reduction in fibrosis after carbon tetrachloride injury, associated w

74 expansion, less inflammation, and decreased fibrosis after CCl(4) injury despite a similar degree of

75 among mammals by showing little scarring or fibrosis after skin or muscle injury, but the Acomys res

76 lated in response to P. aeruginosa by cystic fibrosis airway epithelia.

77 We characterized the fibrosis (amount, architecture, cellular components, and

78 important insights into understanding renal fibrosis and antifibrotic strategies.

79 the progression of human diseases, including fibrosis and cancer.

80 e (NE) activity in tissues, including cystic fibrosis and chronic obstructive pulmonary disease (COPD

81 and right atria increases; and 2) Increased fibrosis and decreased cell-cell coupling due to structu

82 ates for therapeutic applications in cardiac fibrosis and diastolic dysfunction.

83 omal cells from PMF patients correlates with fibrosis and disease severity.

84 Fibrosis and emphysema were present in 66 (17.7%) and 95

85 g neonatal cholangiopathy that progresses to fibrosis and end-stage liver disease by 2 years of age.

86 overall protective effect in lung injury and fibrosis and fit with a mechanism whereby lung lymphatic

87 was positively associated with the stage of fibrosis and HCC.

88 dependent kinase (CDK) complex that promotes fibrosis and hypertrophy.

89 in receptor signalling in mice causes atrial fibrosis and increases susceptibility to atrial fibrilla

90 o it being a key chemokine controlling liver fibrosis and inflammation in the context of YAP/TAZ.

91 ier metabolic profile, including ameliorated fibrosis and inflammation, as well as improved lipid and

92 e of NASH was associated with no decrease in fibrosis and less weight loss (reduction in body mass in

93 ceptive sensitization, bone fracture, muscle fibrosis and muscle fibre loss.

94 ophy/mass (LVM) can be objectively measured, fibrosis and myocyte disarray are difficult to assess.

95 human alcoholic hepatitis (AH) with advanced fibrosis and portal hypertension and in experimental mou

96 pithelial cells, but repair can also lead to fibrosis and progressive kidney disease.

97 The link between liver fibrosis and the natural history of COVID-19 should be e

98 to identify key signalling pathways driving fibrosis and to screen for anti-fibrotic compounds targe

99 nhibits PYCR1 expression, proline synthesis, fibrosis and tumor growth.

100 address the challenges of severe pancreatic fibrosis and young donor age.

101 In carbon tetrachloride-induced fibrosis and zymosan-induced peritonitis models, MVs ame

102 ly infected with HCV, 39 with advanced liver fibrosis, and 20 with mild-moderate liver fibrosis.

103 protective or a pathological role in kidney fibrosis, and about the precise mechanisms and signallin

104 ch include dyskeratosis congenita, pulmonary fibrosis, and aplastic anemia, is characterized by sever

105 ation and a known promoter of cancer growth, fibrosis, and arthritis.

106 nduced cardiac biomarker release, myocardial fibrosis, and atrial fibrillation.

107 Hepatic ductular reactions, pericellular fibrosis, and bridging fibrosis were observed only in th

108 r2(-/-) mice were assessed for liver injury, fibrosis, and ductular reactive (DR) cells.

109 hospho-pyruvate dehydrogenase expression, RV fibrosis, and hypertrophy and improved RV function.

110 ty of human diseases, such as cancer, cystic fibrosis, and inflammatory bowel diseases.

111 sangial cells leads to diabetic nephropathy, fibrosis, and proteinurea, which are inhibited in hepari

112 ing from excessive inward remodeling, medial fibrosis, and thrombosis.

113 macrovascular and microvascular dysfunction, fibrosis, and tissue remodeling are needed and ideally w

114 g of Prox1-deficient tumors, destroyed tumor fibrosis, and unleashed T cell-mediated killing of cance

115 of nonalcoholic steatohepatitis and advanced fibrosis are at markedly increased risk of adverse outco

116 Prevention of progression and reduction in fibrosis are the main aims of treatment.

117 ndards for patient assessment is to use skin fibrosis as an indicator of organ involvement, though th

118 The treatment reduced fibrosis as observed by Sirius red staining, liver hydro

119 ized by myocardial hypertrophy, disarray and fibrosis, as in humans.

120 n-alcoholic fatty liver disease and advanced fibrosis, as well as to detect non-alcoholic steatohepat

121 oline content, and tissue mRNA expression of fibrosis-associated genes (Ccl11, Il13, and Mmp12).

122 the resolution of NASH without worsening of fibrosis at 5 years.

123 ciations of clusters with HFpEF severity and fibrosis biomarkers (PIIINP [procollagen III N-terminal

124 iated with differences in clinical features, fibrosis biomarkers, and functional performance.

125 rgoing atrial fibrillation ablation with low fibrosis burden.

126 BPF99 did not reduce the number of mice with fibrosis but improved collagen proportional area (p < 0.

127 ial events that drive stromal activation and fibrosis by hematopoietic-stromal cross-talk remain elus

128 e model of bleomycin (BLM)-induced pulmonary fibrosis by micro-CT, evaluating longitudinal density ch

129 g, 25% and 42%, respectively, improved liver fibrosis by one stage or more without worsening of steat

130 with bile duct ligation (BDL)-induced liver fibrosis, by monitoring echocardiography and intracardia

131 fragment-based drug discovery and the cystic fibrosis C2-corrector clinical candidate ABBV-3221.

132 Fibrosis can affect any organ and is responsible for up

133 The extent of atrial interstitial fibrosis, cardiomyocyte myocytolysis, cardiomyocyte diam

134 pite therapeutic progress in treating cystic fibrosis (CF) airway disease, airway inflammation with a

135 apeutic approach for the treatment of cystic fibrosis (CF) and other mucoobstructive diseases.Objecti

136 Most infants with cystic fibrosis (CF) have pancreatic exocrine insufficiency tha

137 Cystic fibrosis (CF) is a monogenic disorder caused by mutation

138 pathogens to enter the circulation of cystic fibrosis (CF) patients during chronic infective states h

139 rbidity and mortality associated with cystic fibrosis (CF), a condition that predisposes patients to

140 Background In patients with cystic fibrosis (CF), pulmonary structures with high MRI T2 sig

141 Background In cystic fibrosis (CF), recurrent imaging and pulmonary function

142 duced nephrotoxicity in children with Cystic Fibrosis (CF).

143 We found marked advance of liver fibrosis (chronic damage), as well as necrosis of hepato

144 m advanced liver disease, including bridging fibrosis, cirrhosis, and hepatocellular carcinoma, in th

145 study was to identify risk factors for liver fibrosis/cirrhosis in a cohort of Greek HIV-infected pat

146 vate the expression of proteins that promote fibrosis (collagen type I alpha 1 chain, tissue inhibito

147 Fibrosis commonly occurs during treatment and is associa

148 and fibroblasts from patients with pulmonary fibrosis compared to controls.

149 sion: VCTE is a better biomarker of advanced fibrosis compared with APRI or FIB-4 in HBV/HIV co-infec

150 pertrophy, podocyte injury, and interstitial fibrosis compared with diabetic controls fed normal chow

151 sease-specific differences in adipose tissue fibrosis compared with histologic measures.

152 activation and reduced the severity of liver fibrosis compared with mice given vehicle.

153 ciated with significant reduction in HVPG or fibrosis compared with placebo.

154 AUCs for discriminating advanced fibrosis (CPA >10.3%) were 0.86 (95% CI: 0.76, 0.97), 0.

155 99.3% of patients with AF had ECV below the fibrosis cutoff point (32.8% when converted from MOLLI T

156 Fibrosis decreased, compared with baseline, in samples f

157 s between different liver cells culminate in fibrosis development in NASH, focusing on triggers and c

158 otic liver tissues, rats and mice with liver fibrosis (due to bile duct ligation [BDL] or administrat

159 n regulating biliary proliferation and liver fibrosis during cholestasis.

160 y for test-positives, (2) the enhanced liver fibrosis (ELF) test with hospital liver stiffness measur

161 These findings support the hypothesis that fibrosis, evidenced by increased elastic modulus, is enh

162 fected women) exhibited increased myocardial fibrosis (extracellular volume fraction, 0.34 +/- 0.06 v

163 evidence of reduced spinal inflammation and fibrosis following SCI as compared to C57BL/6 mice (Mus)

164 t Acomys has reduced spinal inflammation and fibrosis following SCI.

165 analysis distinguished idiopathic pulmonary fibrosis from non-idiopathic pulmonary fibrosis ILD and

166 pharmacological tools to inhibit pathologic fibrosis has not been fully evaluated.

167 stic pathways that lead to accelerated liver fibrosis have not been well defined.

168 microbiome as a novel biomarker for advanced fibrosis have only examined patients with nonalcoholic f

169 growth factor-1 (IGF-1) are known to promote fibrosis; however, myofibroblast specific upregulation o

170 onary fibrosis from non-idiopathic pulmonary fibrosis ILD and used lung function to determine the gre

171 ded serum markers and histologic measures of fibrosis improvement and NASH resolution.

172 to be macular atrophy in 60% and subretinal fibrosis in 40%.

173 the pericystic microenvironment, leading to fibrosis in ADPKD.

174 h has a consistent role as a key mediator of fibrosis in all three types of tissue specimen.

175 iotensin II-mediated murine model of cardiac fibrosis in both preventive and therapeutic settings, as

176 rpetual cycles of wounding and healing drive fibrosis in DDEB and RDEB, as well as the formation of a

177 tion potential duration, and reversed atrial fibrosis in diet-induced obese mice as compared with con

178 lysis identified various patterns of macular fibrosis in eyes with nAMD.

179 e is known about the processes that initiate fibrosis in granulomas.

180 sodeoxycholic acid ameliorates ER stress and fibrosis in Grp78 KO mouse and IPF lung slice cultures.C

181 There was also less fibrosis in heart sections from C-dnO1 mice after TAC.

182 e of mitochondrial metabolism of RVfib in RV fibrosis in human and experimental pulmonary arterial hy

183 t the histotype-specific regulation of tumor fibrosis in lung cancer is mediated through differential

184 led that cachectic mice develop perivascular fibrosis in major metabolic organs, including the adipos

185 atment reduced ductular reaction and hepatic fibrosis in Mdr2KO mice, regulating cholangiocyte prolif

186 nd regression of liver necroinflammation and fibrosis in mouse models of non-alcoholic fatty liver di

187 blocking antibody approach attenuated kidney fibrosis in normal mice but not in OASIS knockout mice a

188 Fibrosis in O3-exposed KKAy lungs was confirmed with imm

189 APRI allows screening of NAFLD as well as fibrosis in obese patients.

190 aging time for quantification of LA scar and fibrosis in patients with AF.

191 e biomarkers are used increasingly to assess fibrosis in patients with chronic liver disease.

192 flammation and subsequent failure to resolve fibrosis in response to epithelial injury.

193 reduced aging-related disorders and reduces fibrosis in several diseases.

194 rited susceptibility and clinically apparent fibrosis in SSc skin, and can be an important driver of

195 that results in redox stress and accelerated fibrosis in the aged.

196 The molecular mechanisms regulating fibrosis in the heart are, however, not fully understood

197 ules governing inflammation, thrombosis, and fibrosis in the human interactome (P < 0.001).

198 ctal plate remodeling defects and periportal fibrosis in the liver.

199 lation, macrophage accumulation, and hepatic fibrosis in the Mdr2(-/-) model of cholestasis.

200 (-/-) mice, compared with extensive bridging fibrosis in Tr(-/-)Mdr2(-/-) mice.

201 RNA network that contributes to formation of fibrosis in tumorous and nontumorous organs of mice and

202 nd NAFLD also appeared to have more advanced fibrosis including cirrhosis suggesting a potential syne

203 tageo) diaphragm strength was lower, whereas fibrosis increased, compared with mdx.

204 Liver fibrosis interferes with normal liver function and facil

205 Idiopathic pulmonary fibrosis (IPF) has a poor prognosis and limited treatmen

206 Idiopathic pulmonary fibrosis (IPF) is a disease with high 5-year mortality a

207 Idiopathic pulmonary fibrosis (IPF) is a fatal disease of unknown cause that

208 Idiopathic pulmonary fibrosis (IPF) is characterized by exuberant deposition

209 l to the development of idiopathic pulmonary fibrosis (IPF).

210 n to the development of idiopathic pulmonary fibrosis (IPF).Objectives: We sought to decipher the tra

211 Atrial-tissue fibrosis is a central pathophysiological feature of atri

212 Idiopathic pulmonary fibrosis is a fatal disease involving destruction of the

213 Tissue fibrosis is a hallmark of overuse musculoskeletal injuri

214 Organ fibrosis is a lethal outcome of autoimmune rheumatic dis

215 Myocardial fibrosis is a major determinant of clinical outcomes in

216 Cardiac fibrosis is a pathological process that contributes to t

217 In humans and mice, pulmonary fibrosis is associated with up-regulation of sialidases,

218 re tissue homeostasis in mice in which liver fibrosis is induced chemically or by diet.

219 Fibrosis is the abnormal deposition of extracellular mat

220 The authors hypothesize that muscle fibrosis is the main contributor of breast reconstructio

221 on in chronic liver injury sequelae, such as fibrosis, is unknown.

222 related to tubular injury, inflammation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-4

223 cnn1b-Tg(+)) mice, which recapitulate cystic fibrosis-like mucoinflammatory airway disease, deficient

224 the liver included hepatic steatosis, portal fibrosis, lymphocytic infiltrates and ductular prolifera

225 nd shift work) are associated with pulmonary fibrosis, making them risk factors.

226 Diabetes-associated organ fibrosis, marked by elevated cellular senescence, is a g

227 ed plasma transaminases, reduced biliary and fibrosis markers.

228 Progressive renal pathologies, including fibrosis, mesangial matrix expansion, and tubular hypert

229 In the murine bleomycin-induced lung fibrosis model, GSK3008348 engages alphavbeta6, induces

230 by inflammatory infiltrates (n = 9) and mild fibrosis (n = 8) in the endomysium or replacing muscle f

231 rphotypes of M. abscessus However, in cystic fibrosis neutrophils, wortmannin inhibited killing of a

232 rrhosis, or liver-related death) or advanced fibrosis/non-alcoholic steatohepatitis (NASH) in adult i

233 limited data regarding nephrogenic systemic fibrosis (NSF) risk, but there are few if any unconfound

234 CXCR6 in the development of inflammation and fibrosis of the kidney in salt-sensitive hypertension.

235 acetate (DOCA)/salt-induced inflammation and fibrosis of the kidney.

236 nhibition, with no differences in myocardial fibrosis or cardiac morphometry.

237 nditions such as rheumatoid arthritis, liver fibrosis, or obesity.

238 nd in early compared with advanced stages of fibrosis (P < 0.05 for both).

239 is way to measure CFTR function using cystic fibrosis patient-derived iPSC lines before and after cor

240 1622, both isolated from the lungs of cystic fibrosis patients.

241 pose tissue metabolic dysfunction, including fibrosis, plays a central role in DM pathogenesis.

242 iac magnetic resonance (CMR)-detected atrial fibrosis plus pulmonary vein isolation (PVI).

243 ation approach targeting CMR-detected atrial fibrosis plus PVI was not more effective than PVI alone

244 mechanotransduction pathways associated with fibrosis progression and highlights promising therapeuti

245 en an increase in liver stiffness on MRE and fibrosis progression in NAFLD.

246 use are patient risk factors for accelerated fibrosis progression, yet few randomized controlled tria

247 VD deficiency is associated with liver fibrosis progression.

248 pressed on myeloid cells 2) and displaying a fibrosis-promoting phenotype.

249 Food and Drug Administration-approved cystic fibrosis protein trafficking chaperone, lumacaftor, has

250 Intrareader repeatability in fibrosis quantification was higher for the reference coh

251 7), early injury "R3(injury) " (N = 61), and fibrosis "R4(late) " (N = 8).

252 thesis by showing increased inflammation and fibrosis related gene expression (Serpine 1, Plau, and T

253 ad reduced cytokine production but increased fibrosis relative to control animals.

254 ng and after DAA therapy can improve hepatic fibrosis remains unclear.

255 thrombocytopenia, anasarca, fever, reticulin fibrosis/renal dysfunction, and organomegaly.

256 Organ fibrosis represents a default tissue program activated w

257 st family, the proband presents with hepatic fibrosis, retinitis pigmentosa, and postaxial polydactyl

258 synergistic effect of cardiac dysfunction on fibrosis risk in NAFLD.

259 duals with risk alleles associated with NASH-fibrosis: rs738409C>G in PNPLA3, rs58542926C>T in TM6SF2

260 central pathology committee using the Ishak fibrosis score (F).

261 < .01 for all NITs in F3 and for ELF, NAFLD Fibrosis Score, Fibrosis-4 (FIB-4), and liver stiffness

262 the nonalcoholic fatty liver disease (NAFLD) fibrosis scores (NFS, n = 13,160).

263 PNPLA3 I148M and higher NAFLD liver fat and fibrosis scores were associated with increased liver dis

264 ceae are the main microbiota associated with fibrosis severity in non-obese subjects.

265 Fibrosis, Shc expression, markers of senescence, and nic

266 into the following three groups according to fibrosis stage and a presence or history of hepatic deco

267 eriment, we evaluated the impact of removing fibrosis stage restrictions on hepatitis C (HCV) treatme

268 of LS if compared to patients with the same fibrosis stage.

269 inflammation, hepatocellular ballooning and fibrosis stage.

270 the Pi*ZZ genotype, and increased with liver fibrosis stages.

271 lly expressed proximal tubule lncRNAs during fibrosis suggests they may have unanticipated regulatory

272 However, fibrosis-targeted therapies are currently limited.

273 -exposed patients displayed higher levels of fibrosis than those from nonexposed patients.

274 c disorder caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene

275 cleotide-binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) have

276 goblet cells, motile ciliated cells, cystic fibrosis transmembrane conductance regulator (CFTR)-rich

277 Rationale: Enhancing non-CFTR (cystic fibrosis transmembrane conductance regulator)-mediated a

278 ns of focal glomerulosclerosis, interstitial fibrosis, tubular atrophy and arteriolosclerosis.

279 inical characteristics included interstitial fibrosis/tubular atrophy, larger cortical nephron size (

280 nance sensor for grading liver steatosis and fibrosis using diffusion-weighted multicomponent T2 rela

281 ere either healthy or affected by myocardial fibrosis using X-ray microtomography.

282 Associations between NASH-fibrosis variants and metabolites were assessed using li

283 Fibrosis was accelerated in older mice on FFD, and Shc i

284 Fibrosis was categorized using spectral-domain OCT with

285 No significant inflammation or fibrosis was found in adjacent liver tissues of 3 patien

286 NASH resolution with no worsening of fibrosis was observed in 24% of patients given aldafermi

287 ospectively included when macular subretinal fibrosis was present.

288 However, fibrosis was primarily periductular in Mdr2(-/-) mice, c

289 Fibrosis was segmented and quantified based on compariso

290 Fibrosis was staged by a central pathology committee usi

291 In adipose tissue biopsies, changes in fibrosis were evaluated by immunohistological examinatio

292 irway hyperresponsiveness, inflammation, and fibrosis were exclusively present in female BMC mice wit

293 actions, pericellular fibrosis, and bridging fibrosis were observed only in the LivKO mice.

294 lated esophageal necrosis, inflammation, and fibrosis were seen in all radiofrequency sections, as co

295 2, and PKC-alpha/delta expression and atrial fibrosis were significantly increased in diet-induced ob

296 al cutoff values for distinguishing advanced fibrosis were used to assess treatment response.

297 erbated the development of bleomycin-induced fibrosis, whereas mutation of REVERBalpha in club or mye

298 HE4 overexpression in hypoxia-induced renal fibrosis will provide important insights into understand

299 5% confidence interval, 0.91-0.99) and F2-F4 fibrosis with an area under the curve of 0.88 (95% confi

300 e, which in the advanced stages evolves into fibrosis without detectable inflammation.