ライフサイエンスコーパス: fibrosis

1 many respiratory diseases, including cystic fibrosis.

2 Overall, 113 patients (30.9%) had F2-4 fibrosis.

3 lic dysfunction and comparable intra-cardiac fibrosis.

4 the effect of these potential biomarkers of fibrosis.

5 t (PAI-1(-/-)) mice developed severe cardiac fibrosis.

6 ies as the predictor of future liver fat and fibrosis.

7 atients, all of which present high levels of fibrosis.

8 therapeutic approach for attenuating kidney fibrosis.

9 lasts are deemed the main executors of organ fibrosis.

10 e RNA-Sequencing study in human conjunctival fibrosis.

11 a new profibrotic mediator in lung and skin fibrosis.

12 orroborating the selective in vivo effect on fibrosis.

13 ived little attention in the study of SSc or fibrosis.

14 ncreased macrophage infiltration, and tissue fibrosis.

15 significant role in hepatic inflammation and fibrosis.

16 t alveolar macrophages did not contribute to fibrosis.

17 nscriptional effects that lead to myocardial fibrosis.

18 fibrosis than in patients with grade 1 or 2 fibrosis.

19 d into those with fibrosis and those without fibrosis.

20 d with the development of tubulointerstitial fibrosis.

21 , including inflammation, tolerance, or even fibrosis.

22 e death, inflammation, and progressive liver fibrosis.

23 roved cardiac function, and tended to reduce fibrosis.

24 antly reduced biomarkers of inflammation and fibrosis.

25 astasis in breast cancer by preventing tumor fibrosis.

26 l and attractive therapeutic target in liver fibrosis.

27 SFs from fibrotic tissue to ameliorate liver fibrosis.

28 f a noninvasive image-based measure of renal fibrosis.

29 ppression for the treatment of skin and lung fibrosis.

30 diabetes kidney, and whether H2S ameliorates fibrosis.

31 g candidate for in vivo imaging of pulmonary fibrosis.

32 osis have a 12 times higher risk of advanced fibrosis.

33 hospital-acquired infections or with cystic fibrosis.

34 (serving as the first hit) - into pathogenic fibrosis.

35 ake in the fibrotic kidney and reduced renal fibrosis.

36 acking alpha-granules and progressive marrow fibrosis.

37 veral respiratory diseases, including cystic fibrosis.

38 n response to myocardial strain and possibly fibrosis.

39 -weighted MR imaging in the staging of liver fibrosis.

40 cting ROCK inhibitor (AMA0825) on intestinal fibrosis.

41 e used to evaluate characteristics of atrial fibrosis.

42 ses non-alcoholic steatohepatitis (NASH) and fibrosis.

43 renal dysfunction, injury, inflammation, and fibrosis.

44 the neonates developed nephrogenic systemic fibrosis.

45 y of the imaging parameters in staging liver fibrosis.

46 ate cells to promote the resolution of liver fibrosis.

47 e in the hepatoprotection conferred by liver fibrosis.

48 eventual lethality in the absence of cardiac fibrosis.

49 regulator (CFTR) mutation that causes cystic fibrosis.

50 ated creatine kinase activity and endomysial fibrosis.

51 obstructive pulmonary disease, and pulmonary fibrosis.

52 ial cell regeneration and lung repair during fibrosis.

53 veloped for treatment of patients with liver fibrosis.

54 trophy and disarray, as well as interstitial fibrosis.

55 ith crenolanib attenuated the skin and heart fibrosis.

56 PF and mice with bleomycin-induced pulmonary fibrosis.

57 the protective effect of SphK2 deficiency in fibrosis.

58 e formation observed in patients with cystic fibrosis.

59 vity of C5L2 in infection-induced peritoneal fibrosis.

60 tly no therapies to directly inhibit hepatic fibrosis.

61 s to hepatic inflammation and early signs of fibrosis.

62 % (95% CI, 0.2-7.5) of persons with moderate fibrosis, 4.7% (95% CI, 1.5-14.1) with severe fibrosis,

63 NASH is actively remodeled even in advanced fibrosis, a disease that is generally regarded as static

64 ality were elevated in persons with moderate fibrosis (adjusted hazard ratio [aHR], 1.42 [95% confide

65 was the only factor associated with advanced fibrosis (adjusted OR, 1.044; P = 0.025).

66 late graft function and reduced interstitial fibrosis after transplant.

67 basement membrane thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased

68 l in CFTR(-/-) swine, suggesting that cystic fibrosis airways do not respond to inhaled pathogens, th

69 d skeletal muscle phenotype with significant fibrosis, an effect consistent with increased levels of

70 the atria, MEF2A regulated genes involved in fibrosis and adhesion, whereas in the ventricles, it con

71 racellular matrix, inducing local pancreatic fibrosis and an inflammatory response.

72 mechanisms and effector molecules triggering fibrosis and angiogenesis in SM.

73 ptosis are important in idiopathic pulmonary fibrosis and asbestosis.

74 Because LH2 promotes fibrosis and cancer metastasis, our findings suggest tha

75 osinusitis, and exacerbations of both cystic fibrosis and chronic obstructive pulmonary disease.

76 e protected against bleomycin (BLEO)-induced fibrosis and collagen deposition.

77 ive repair after AKI may lead to progressive fibrosis and decline in kidney function.

78 otes inflammation, a process contributing to fibrosis and decline in organ function.

79 e the association between diffuse myocardial fibrosis and diastolic dysfunction.

80 C(low) MPs may contribute to the progressive fibrosis and dysfunction of mdx(5cv) diaphragm.

81 sts similarly inhibited the gene program for fibrosis and extracellular matrix remodeling, although d

82 HD patients display diffuse myocarditis with fibrosis and hypertrophy.

83 meliorating hemodynamic load-induced cardiac fibrosis and identified its intracellular target.

84 by the presence of pleural and peribronchial fibrosis and impaired lung mechanics determined by the f

85 of interventricular septum and interstitial fibrosis and increases anterior wall thickness and cardi

86 Mif deletion or MIF inhibition also worsened fibrosis and inflammation and associated with worse kidn

87 cing multiple functions including apoptosis, fibrosis and inflammation.

88 pathology of lymphedema by promoting tissue fibrosis and inhibiting lymphangiogenesis.

89 xb, are critical in development of pulmonary fibrosis and may be a paradigm for the regulation of tis

90 CCl4 produced similar fibrosis and necroinflammation and increased the mRNA an

91 (TE) can be used in noninvasive diagnosis of fibrosis and steatosis in patients with nonalcoholic fat

92 fibroblasts are protected from skin and lung fibrosis and that a disintegrin and metalloproteinase 10

93 he participants were divided into those with fibrosis and those without fibrosis.

94 chlamydial infection include fallopian tube fibrosis and tubal factor infertility.

95 ic histological damage of which interstitial fibrosis and tubular atrophy are dominant features.

96 This was accompanied by cardiac fibrosis and up-regulation of NFAT-c2, reflecting increa

97 ents 12 years of age or older who had cystic fibrosis and were heterozygous for the Phe508del mutatio

98 fibrosis has progressed to at least moderate fibrosis and, in some cases, cirrhosis.

99 ly depicts the presence of significant liver fibrosis and, less accurately, mild liver fibrosis in pe

100 logic features (steatosis, inflammation, and fibrosis) and modified nonalcoholic steatohepatitis cate

101 ibrosis, 4.7% (95% CI, 1.5-14.1) with severe fibrosis, and 16.3% (95% CI, 7.0-35.1) with cirrhosis (P

102 Levels of airway inflammation, mucus, fibrosis, and airway smooth muscle were no different in

103 sis results in systemic inflammation, tissue fibrosis, and autoimmunity.

104 0% (95% CI, 33.0-67.7) with moderate, severe fibrosis, and cirrhosis, respectively (P < 0.01).

105 h ethanol-induced liver disease and advanced fibrosis, and controls, were given injections of recombi

106 gical myofibroblast activation, interstitial fibrosis, and HF progression.

107 e in ROS levels, and reduced cell apoptosis, fibrosis, and hypertrophy in H9c2 cells.

108 uced long-term left ventricular dysfunction, fibrosis, and hypertrophy in naive recipient mice.

109 response to injury is a key step in hepatic fibrosis, and is characterized by trans-differentiation

110 Dysregulation of this process can lead to fibrosis, and LOXL2 is known to be upregulated in fibrot

111 oved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches will t

112 ion, blocked the development of interstitial fibrosis, and prevented immune cell infiltration.

113 h) mice, IBDM, proliferation, HSC activation/fibrosis, and TGF-beta1 expression/secretion were decrea

114 sis, global glomerulosclerosis, interstitial fibrosis, and tubular atrophy) all increase with age.

115 myelofibrosis; kidney-, pancreas-, and heart-fibrosis; and nonalcoholic steatohepatosis converge in t

116 ssion of proinflammatory cytokines), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adeno

117 Glomerulosclerosis and tubulointerstitial fibrosis are associated with lower renal parenchymal ela

118 hrombosis, inflammation, cardiac injury, and fibrosis are introduced in the context of their pathophy

119 utrophilic airway diseases, including cystic fibrosis, are characterized by excessive neutrophil infi

120 ith the use of non-invasive markers of liver fibrosis, are needed in the general population setting.

121 can be used to distinguish inflammation from fibrosis at early stages of disease, even before the dev

122 brotic mice arrested the progression of lung fibrosis, attenuated cellular apoptosis (caspase-3/7) an

123 inium enhancement, indicative of ventricular fibrosis, before randomization to either CA or ongoing M

124 Bone marrow fibrosis (BMF) develops in various hematological and non

125 tent antifibrotic effects in models of adult fibrosis, but the mechanisms of action are unclear.

126 are key players in the development of liver fibrosis, but the role of PNPLA3 and its variant I148M i

127 SIRT3 deficiency promotes lung fibrosis by augmenting alveolar epithelial cell mitochon

128 ressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH

129 ypertrophy, reduced cardiomyocyte apoptosis, fibrosis, calcium/calmodulin-dependent protein kinase II

130 alcoholic steatohepatitis (NASH) and hepatic fibrosis, can be used for patients with psoriasis to aid

131 In the heart, fibrosis causes mechanical and electrical dysfunction an

132 RATIONALE: Individuals with cystic fibrosis (CF) experience frequent acute pulmonary exacer

133 ardiac fibroblasts (CFBs) to promote cardiac fibrosis (CF) in nonischemic heart failure (HF).

134 a rarely reported in patients without cystic fibrosis (CF) or immunocompromising conditions.

135 In cystic fibrosis (CF) patients, chronic airway infection by Pseu

136 is an important diagnostic marker for cystic fibrosis (CF), but the implementation of point-of-care s

137 ular pathogen killing is defective in cystic fibrosis (CF), despite abundant production of reactive o

138 sis, pneumonia, wound infections, and cystic fibrosis (CF), which is caused by mutations of the cysti

139 characterize the chronic lung disease cystic fibrosis (CF).

140 is and progression of lung disease in cystic fibrosis (CF).

141 he lung, pancreas and other organs in cystic fibrosis (CF).

142 A hallmark of CKD progression is renal fibrosis characterized by excessive accumulation of extr

143 yomavirus load levels and Banff interstitial fibrosis ci scores.

144 Moderate/severe interstitial fibrosis (ci>/=2) at 1 year was observed in 4.2% of pati

145 th problem around the world and often causes fibrosis/cirrhosis and hepatocellular carcinoma.

146 atients were more likely to have significant fibrosis/cirrhosis at 1 year on ART.

147 asson trichrome stain), molecular markers of fibrosis (collagen and transforming growth factor-beta)

148 erfusion and CD31 expression, while reducing fibrosis compared to saline.

149 lly, TANGO1(+/-) mice displayed less hepatic fibrosis compared to WT mice in two separate murine mode

150 bination and extent of hepatic inflammation, fibrosis, congestion, and portal hypertension.

151 ing the detrimental health effects of cystic fibrosis could be the identification of proteins whose s

152 erval [CI]: 0.4-6.8) of persons with no/mild fibrosis developed ESLD compared with 7.9% (95% CI, 4.0-

153 were performed in the context of the cystic fibrosis diagnosis and preliminary investigation of the

154 a, aplastic anemia, and idiopathic pulmonary fibrosis disrupt the binding between the protein subunit

155 lpha) play key roles in progression of renal fibrosis, dual blockade of TGF-beta1 and TNF-alpha is de

156 s, we hypothesized that PAI-1 also regulates fibrosis during cardiac injury.

157 ients, to help monitor for risk of worsening fibrosis during MTX therapy.

158 tive correlations between biliary periductal fibrosis during opisthorchiasis and CagA and CagA with C

159 l hematologic malignancy characterized by BM fibrosis, extramedullary hematopoiesis, circulating CD34

160 reased RV native T1 suggestive of diffuse RV fibrosis, for which volume loading seems to be a risk fa

161 lasts and the molecular mechanisms governing fibrosis formation and resolution.

162 genic populations of lung fibroblasts during fibrosis formation and resolution.

163 the first 12 months of life at 28 US Cystic Fibrosis Foundation-accredited Care Centers from January

164 ells in vitro, we evaluated angiogenesis and fibrosis gene expression.

165 tion of miR-200b decreased the expression of fibrosis genes in vitro in cholangiocyte and HSC lines.

166 Fibrosis had a weaker independent association with the a

167 % (95% CI, 0.0-14.8) of persons with no/mild fibrosis had suffered an LRD compared with 1.0% (95% CI,

168 2/3 signaling in fibroblast-mediated cardiac fibrosis has not been directly evaluated in vivo.

169 integrin and Src kinase interaction to lung fibrosis has not been mechanistically investigated.

170 cost, treatment is often denied until liver fibrosis has progressed to at least moderate fibrosis an

171 Proteomic comparison of lung and skin fibrosis identified a common upregulation of marginal zo

172 ssue homeostasis but can lead to allergy and fibrosis if not adequately regulated.

173 served in diverse disorders, such as cancer, fibrosis, immune dysregulation, and neurodegenerative di

174 to discover and quantify diffuse myocardial fibrosis in 25 individuals with SCA (mean age, 23 +/- 13

175 techniques to more accurately stage hepatic fibrosis in a rat model.

176 o reduce these effects and potentially treat fibrosis in addition to hypertension.

177 to assess its ability to help quantify liver fibrosis in animal models.

178 d replicated, five also associate with renal fibrosis in biopsies from CKD patients and show concorda

179 treatment can achieve a regression of liver fibrosis in chronic HEV patients.

180 n attractive new target for the treatment of fibrosis in chronic kidney disease.

181 R-194-dependent MMPs and PARP-1 causes renal fibrosis in diabetes kidney, and whether H2S ameliorates

182 rove the myogenesis of stem cells and reduce fibrosis in dKO muscle.

183 pharmacological inhibition, ameliorate skin fibrosis in experimental mouse models.

184 to prospectively assess the risk of advanced fibrosis in first-degree relatives of probands with NAFL

185 unication in the activation of HSC for liver fibrosis in HCV infection.IMPORTANCE HCV-associated live

186 the tubular apoptosis and renal interstitial fibrosis in kidney diseases.

187 ot different (P > 0.05) for identifying F2-4 fibrosis in low and high-replicative patients.

188 Fibrosis in lung and skin leads to progressive bronchiol

189 PAI-1 is an essential repressor of cardiac fibrosis in mammals.

190 suppressive role during spontaneous cardiac fibrosis in multiple species, we hypothesized that PAI-1

191 stography (VCTE) in the detection of hepatic fibrosis in patients with severe to morbid obesity.

192 er fibrosis and, less accurately, mild liver fibrosis in pediatric patients with nonalcoholic fatty l

193 identify miR-21 as an important effector of fibrosis in the peritoneal membrane, and a promising bio

194 ivers, suggesting an important role of liver fibrosis in the premalignant environment (PME) of the li

195 sis and nonalcoholic steatohepatitis without fibrosis in the reference comparison group.

196 hancing TLR2-mediated inflammation increased fibrosis in vivo Furthermore, soluble TLR2 (sTLR2), a ne

197 ed with significant fibrosis (versus mild/no fibrosis) in multivariable analysis included higher leve

198 factors known to predict and drive allograft fibrosis include graft quality, inflammation (whether "n

199 ates of false-positive LSM results for F3-F4 fibrosis increased according to CAP tertiles (7.2% in lo

200 miR-155(-/-) mice developed exacerbated lung fibrosis, increased collagen deposition, collagen 1 and

201 of serelaxin on cardiac and renal function, fibrosis, inflammation and lipid accumulation were studi

202 rpose To determine the relationship of liver fibrosis, inflammation, and steatosis with the magnetic

203 Fibrosis involves increasing amounts of scar tissue appe

204 Fibrosis involves the production of extracellular matrix

205 patients diagnosed with idiopathic pulmonary fibrosis (IPF) in clinical practice could participate in

206 Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease wit

207 Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal fibro

208 Idiopathic pulmonary fibrosis (IPF) is a disease characterized by the accumul

209 Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial l

210 Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial p

211 Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a prevalenc

212 ial community influence idiopathic pulmonary fibrosis (IPF) progression.

213 Tubulointerstitial fibrosis is a chronic and progressive process affecting

214 CV infection.IMPORTANCE HCV-associated liver fibrosis is a critical step for end-stage liver disease

215 Lung fibrosis is an unabated wound healing response character

216 ue remodeling and respiratory disease.Cystic fibrosis is caused by mutations in the CFTR chloride cha

217 Cholestatic liver fibrosis is caused by obstruction of the biliary tract a

218 Myocardial fibrosis is linked with adverse clinical outcomes in adu

219 Bone marrow fibrosis is the result of a complex and not yet fully un

220 alyses of B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource for und

221 AOC3 contributes to the development of lung fibrosis mainly by regulating the accumulation of pathog

222 Our findings demonstrated that liver fibrosis manifested a beneficial role for host survival

223 osed macrophages, activates inflammasome and fibrosis markers in HSCs and that neutralizing antibody

224 ed HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in serum and tissues, and improved live

225 tologically detectable necroinflammation and fibrosis (mean damping ratio at 80 Hz and 20-week feedin

226 To investigate whether myocardial fibrosis (MF) is similarly prevalent both in those with

227 Quantifying myocardial fibrosis (MF) with myocardial extracellular volume measu

228 ith several human diseases, including tissue-fibrosis, neurodegeneration and cancer.

229 erse effects, including nephrogenic systemic fibrosis (NSF), the untreatable condition recently linke

230 Hepatic fibrosis occurs during the progression of primary sclero

231 n our understanding of two CCDDs, congenital fibrosis of the extraocular muscles (CFEOM) and Duane re

232 ial Gal-3 expression correlated with cardiac fibrosis on left ventricular biopsy (P=0.63; P<0.01).

233 was cost-effective only for patients with F3 fibrosis; our results highlight the promise of bariatric

234 hemical makeup of a human lung from a cystic fibrosis patient.

235 Peritoneal fibrosis (PF) is a serious complication in various clini

236 Patients with pancreatic-insufficient cystic fibrosis (PI-CF) are at increased risk for developing di

237 d with targeting downstream inflammatory and fibrosis processes.

238 ssociated with the severity of hepatitis and fibrosis progression during chronic hepatitis C infectio

239 d conditions or demographics known to impact fibrosis progression in NAFLD and the inclusion of patie

240 e that hepatic inflammation, fibrosis stage, fibrosis progression rate, hepatic infiltration of immun

241 ot substantially associated with accelerated fibrosis progression, whereas drinking >14 drinks per we

242 14 drinks per week showed increased rates of fibrosis progression.

243 Myocardial fibrosis quantified by extracellular volume (ECV) CMR me

244 ores on the respiratory domain of the Cystic Fibrosis Questionnaire-Revised, a quality-of-life measur

245 Fibrosis rate was evaluated within each woman as she tra

246 cretory response to the inhalation of cystic fibrosis relevant bacteria.

247 entiation/activation in idiopathic pulmonary fibrosis remain poorly understood.

248 served a myogenic-to-lipogenic switch during fibrosis resolution.

249 Intestinal fibrosis resulting in (sub)obstruction is a common compl

250 nt of insoluble aggregates, decreases muscle fibrosis, reverts muscle strength to the level of health

251 and positive correlation with the degree of fibrosis (Rho = 0.430, P = 0.0044), while the routinely

252 management with common clinical measures of fibrosis risk stratification merits further investigatio

253 holic fatty liver, positive correlation with fibrosis score and liver stiffness) and correlated with

254 ex was an independent risk factor for higher fibrosis score in AS valves (P=0.003).

255 ffects, and monitor for worsening of hepatic fibrosis scores during MTX therapy.

256 n the United States population, higher liver fibrosis scores were associated with increased liver dis

257 erall mortality was also greater with higher fibrosis scores.

258 Indeed, protein levels of fibrosis signaling mediator TGF-beta remained the same a

259 Using fibrosis stage 0 as a reference population, fibrosis sta

260 creased QALYs for all patients regardless of fibrosis stage, but was cost-effective only for patients

261 We demonstrate that hepatic inflammation, fibrosis stage, fibrosis progression rate, hepatic infil

262 clearance irrespective of HIV, diabetes, or fibrosis stage, whereas lipid alterations may warrant fu

263 fibrosis stage 0 as a reference population, fibrosis stage-specific mortality rate ratios (MRRs) wit

264 therapy in coinfected patients regardless of fibrosis stage.

265 for obese patients with NASH, regardless of fibrosis stage; in overweight patients, surgery increase

266 niversal," treat all patients, regardless of fibrosis stage; policy 2, treat only "prioritized" patie

267 A costs, in the utility value of patients in fibrosis stages F0-F3 post-sustained virological respons

268 tant pulmonary pathogen especially in cystic fibrosis sufferers.

269 Neddylation inhibition reduces fibrosis, suggesting neddylation as a potential and attr

270 reas was much lower in patients with grade 3 fibrosis than in patients with grade 1 or 2 fibrosis.

271 As a consequence, in subjects with F0-F2 fibrosis, the rates of false-positive LSM results for F3

272 e essential for C. muridarum to induce tubal fibrosis; this may be induced by the gastrointestinal C.

273 the development and progression of pulmonary fibrosis through its regulation of ADORA2B expression on

274 rrhizin ameliorates bleomycin-induced dermal fibrosis through the inhibition of fibroblast activation

275 HSCs mediate hepatic fibrosis through their activation from a quiescent state

276 homologous to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFTR or AB

277 Inappropriate activation of the cystic fibrosis transmembrane conductance regulator (CFTR) chlo

278 Mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene

279 action of modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFTR) is k

280 , which is caused by mutations of the cystic fibrosis transmembrane conductance regulator (Cftr).

281 W1282X is the fifth most common cystic fibrosis transmembrane regulator (CFTR) mutation that ca

282 d GFR (P<0.001) and presence of interstitial fibrosis/tubular atrophy (P=0.003) at diagnosis and chan

283 The prevalence of liver fibrosis varied between 0.7% and 25.7%.

284 Biomarkers associated with significant fibrosis (versus mild/no fibrosis) in multivariable anal

285 Myocardial fibrosis was detected to a significantly lower degree in

286 Bridging fibrosis was noted in 20.6% of patients but no patients

287 A gradual regression of liver fibrosis was reported (Metavir A0/F1 in 2015 versus A3/F

288 Fibrosis was subsequently measured ex vivo by means of h

289 this, a decisional flowchart for predicting fibrosis was suggested by combining both LSM and CAP val

290 efforts to generate a new medicine for liver fibrosis, we sought to identify improved small molecule

291 s for the association of any and significant fibrosis were 0.92 (95% confidence interval [CI]: 0.86,

292 g levels of diethylnitrosamine-induced liver fibrosis were imaged before and 45 minutes after injecti

293 monocyte-derived alveolar macrophages during fibrosis were up-regulated in human alveolar macrophages

294 inning of CKD significantly aggravated renal fibrosis, whereas it did not lead to renal dysfunction.

295 eir recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages d

296 gressive kidney disease are characterized by fibrosis whereby the prototypical prosclerotic growth fa

297 -cell infiltration in the skin that leads to fibrosis, which can be life-limiting.

298 me, these mice develop spontaneous pulmonary fibrosis, which is ameliorated by restoration of lung ch

299 olonoscopy strategy for patients with cystic fibrosis who never received an organ transplant; this st

300 2 cells and B. abortus induces autophagy and fibrosis with concomitant apoptosis of LX-2 cells, which