ライフサイエンスコーパス: airway remodeling

1 miR-98) and PPARgamma levels, thus promoting airway remodeling.

2 man lung fibroblasts (HLFs) is implicated in airway remodeling.

3 ation, airway hyperresponsiveness (AHR), and airway remodeling.

4 rotein YKL-40 has been related to asthma and airway remodeling.

5 to allergic inflammation, AHR, and fibrotic airway remodeling.

6 are cardinal features of asthma and initiate airway remodeling.

7 d elastance), eosinophilic inflammation, and airway remodeling.

8 can express factors that drive subepithelial airway remodeling.

9 ogression of morphologic emphysema and small airway remodeling.

10 ing its salutary effects on fibrinolysis and airway remodeling.

11 duration) and the development of subsequent airway remodeling.

12 grity, diminished lung function and impaired airway remodeling.

13 HT may be targeted to prevent asthma-related airway remodeling.

14 luated for cellular features associated with airway remodeling.

15 s of eosinophilic inflammation and levels of airway remodeling.

16 d which may play a key role in mechanisms of airway remodeling.

17 ration in airway smooth muscle function, and airway remodeling.

18 ry and profibrotic agents that contribute to airway remodeling.

19 tion, TGF-beta1 and collagen expression, and airway remodeling.

20 te and chronic lung diseases associated with airway remodeling.

21 , allergic and nonallergic inflammation, and airway remodeling.

22 e immunodeficient and display increased lung airway remodeling.

23 F-beta and thereby ameliorating pathological airway remodeling.

24 ines are neutralized to define their role in airway remodeling.

25 duced lung inflammatory responses as well as airway remodeling.

26 ressing TGF-beta1 to the airway and enhanced airway remodeling.

27 al derived NF-kappaB regulated chemokines in airway remodeling.

28 consistent pathologic component of asthmatic airway remodeling.

29 enes that may contribute to allergen-induced airway remodeling.

30 pithelial chimerism was also associated with airway remodeling.

31 y and might serve as a novel target to blunt airway remodeling.

32 eased by day 14 p.i. and was associated with airway remodeling.

33 5, eosinophils, alphaVbeta6, and TGF-beta in airway remodeling.

34 scin reflects disease activity in asthma and airway remodeling.

35 Asthma is associated with airway remodeling.

36 unologic (busulfan) method, markedly reduced airway remodeling.

37 ween allergic inflammation and initiation of airway remodeling.

38 ve profound effects on ASM cell function and airway remodeling.

39 d/or parenchymal changes as well as proximal airway remodeling.

40 that impairment of this function may augment airway remodeling.

41 el therapeutic approach in the management of airway remodeling.

42 e immunologic events leading to inflammatory airway remodeling.

43 odulates ASM cell proliferation and leads to airway remodeling.

44 ventional therapies, defining the concept of airway remodeling.

45 oscopic treatment for severe asthma, targets airway remodeling.

46 tion and transcriptomic pathways involved in airway remodeling.

47 ions by quelling persistent inflammation and airway remodeling.

48 beta and IL-6 signaling that are relevant to airway remodeling.

49 signature enriched in genes associated with airway remodeling.

50 SV lower respiratory tract infection-induced airway remodeling.

51 landin E2 synthesis has been associated with airway remodeling.

52 irway inflammation, hyperresponsiveness, and airway remodeling.

53 mice were protected from D. farinae-induced airway remodeling.

54 that modify the immune response and trigger airway remodeling.

55 load, and prevented type 2 inflammation and airway remodeling.

56 peribronchiolar inflammation, and structural airway remodeling.

57 ory cells, cytokine signatures, and fibrotic airway remodeling.

58 obacco smoke exposure on lung parenchyma and airway remodeling.

59 ey have not been shown to directly influence airway remodeling.

60 ronchoconstriction, airway inflammation, and airway remodeling.

61 response, and SEMA3D has a plausible role in airway remodeling.

62 did not alter airway hyperresponsiveness or airway remodeling.

63 asthma is characterized by inflammation and airway remodeling.

64 to corticosteroid therapy and show increased airway remodeling.

65 a before the development of inflammation and airway remodeling.

66 ensitivity, the epithelial cell profile, and airway remodeling.

67 oodborne progenitor cells may participate in airway remodeling.

68 ctoside-binding lectin galectin-3 (Gal-3) in airway remodeling, a characteristic feature of asthma th

69 matrix deposition and fibrosis in asthmatic airways remodeling, a pathologic process still without e

70 We sought to compare QCT parameters of airway remodeling, air trapping, and emphysema between a

71 ent exacerbations of allergic asthma lead to airway remodeling and a decrease in pulmonary function,

72 Computed tomography (CT)-assessed proximal airway remodeling and air trapping in asthmatic patients

73 Airway remodeling and airway hyperresponsiveness are cen

74 ammatory response to ovalbumin from those of airway remodeling and airway hyperresponsiveness, illust

75 factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness.

76 tly cited as important for the mechanisms of airway remodeling and airway hyperresponsiveness.

77 highlighted in the section on asthma include airway remodeling and anti-inflammatory therapy, leukotr

78 expression in the airway and contributes to airway remodeling and asthma severity.

79 e to inflammation, adversely effecting lower airway remodeling and asthma severity.

80 Pathways of airway remodeling and cellular inflammation are associat

81 retion of mucus is an important component of airway remodeling and contributes to the mucus plugs and

82 by enzyme-linked immunosorbent assay, while airway remodeling and cytokine production were studied b

83 ed with the susceptibility to COPD including airway remodeling and emphysema in genome-wide associati

84 Airway remodeling and emphysema were determined morphome

85 thout PH and to correlate CT measurements of airway remodeling and emphysema with PH.

86 We determined the genes associated with airway remodeling and eosinophilic inflammation in patie

87 lecular targets for the treatment of chronic airway remodeling and fibrosis in asthma.

88 Asthma is characterized by airway remodeling and hyperreactivity.

89 ared biological roles of ORMDLs, influencing airway remodeling and hyperresponsiveness.

90 However, airway remodeling and inflammation have not been extensi

91 wall thickness (WT-Pi10) was used to assess airway remodeling and low lung area percentage (LAA%) to

92 pletion and corticosteroid administration on airway remodeling and lung function were examined.

93 B cells in the control of lung function and airway remodeling and may support future concepts for B-

94 is required for mucosal inflammation-coupled airway remodeling and myofibroblast expansion in the mou

95 Induction in the mature lung caused airway remodeling and peribronchiolar nodules, but alveo

96 based airway SA/V is an imaging biomarker of airway remodeling and provides differential information

97 considerable evidence of lesion healing and airway remodeling and reestablishment.

98 airway hyperresponsiveness, but its role in airway remodeling and steroid resistance is unknown.

99 zing antibodies to SCF significantly reduced airway remodeling and suppressed the recruitment of thes

100 lavage eosinophil composition and suppressed airway remodeling and T cell migration into the lung in

101 tered as anti-inflammatory therapy may favor airway remodeling and therefore be detrimental.

102 e to stop progression of emphysema and small airway remodeling and to partially protect against pulmo

103 unique role for TRPV4 in D. farinae-induced airway remodeling and warrant further studies in humans

104 The latter has worse small airways remodeling and narrowing, which account for the

105 tokine production, immunoglobulin synthesis, airway remodeling, and bronchial hyperreactivity were me

106 ithelium, leading to allergic sensitization, airway remodeling, and eosinophilic inflammation in mous

107 eness (AHR), reversible airflow obstruction, airway remodeling, and episodic exacerbations caused by

108 tamin D are associated with asthma severity, airway remodeling, and exacerbation rate increase, espec

109 acterized by inflammation, mucus metaplasia, airway remodeling, and hyperresponsiveness.

110 bs (e.g., IgG1, IgE, and IgA), eosinophilia, airway remodeling, and hyperresponsiveness; all pathophy

111 our understanding of the molecular basis of airway remodeling, and identify novel therapeutic target

112 way increase expression of genes relevant to airway remodeling, and increase the collagen synthesis o

113 neutrophilic and eosinophilic inflammation, airway remodeling, and lung expression of several cytoki

114 Airway remodeling (AR) is a prominent feature of asthma

115 Epithelial damage and airway remodeling are consistent features of bronchial a

116 ion, extracellular matrix (ECM) changes, and airway remodeling are described in PSW and SA, the under

117 is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airwa

118 nduced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.

119 ucus metaplasia, subepithelial fibrosis, and airway remodeling are significantly augmented.

120 Inflammation and airway remodeling are two responses readily apparent in

121 c airway inflammation and fibrosis, known as airway remodeling, are defining features of chronic obst

122 ctural alterations, variously referred to as airway remodeling, are well documented in the asthmatic

123 tional endotoxin exposure to parenchymal and airway remodeling as defined by quantitative computed to

124 c stem cells, is important in the process of airway remodeling as well.

125 3 signaling is required for allergen-induced airway remodeling, as well as allergen-induced accumulat

126 smooth muscle (ASM) cells may contribute to airway remodeling associated with asthma.

127 of pathways related to ciliary function and airway remodeling at 3 dpi and serine-type endopeptidase

128 hat adaptive T cell immunity is required for airway remodeling because mice deficient in alpha/beta T

129 Airway remodeling burden is not limited to airflow limit

130 that eosinophils contribute substantially to airway remodeling but are not obligatory for allergen-in

131 ay inflammation, goblet cell metaplasia, and airway remodeling, but all of these features in this vir

132 Angiogenesis is a consistent feature of airway remodeling, but its contribution to pathophysiolo

133 Finally, Lyn may critically regulate airway remodeling by directly interacting with TGF-beta3

134 TRPC1 intensifies house dust mite-induced airway remodeling by facilitating epithelial-to-mesenchy

135 may play an important role in the process of airway remodeling by promoting the proliferation of airw

136 nterleukin-31 may play a significant role in airway remodeling by promoting the recruitment of bone m

137 This allergen-induced airway remodeling can be replicated in a mouse asthma mo

138 sistent asthma and asthma exacerbations; (3) airway remodeling: clinical consequences and reversibili

139 antification of emphysema, CT measurement of airway remodeling correlates with PAPm and could be used

140 onary disease (COPD) that has developed from airway remodeling due to asthma, as compared with other

141 Contributions of mechanical signals to airway remodeling during asthma are poorly understood.

142 nophils and suggest a potential mechanism of airway remodeling during chronic disease.

143 iferation of ASM directly contributes to the airway remodeling during development of lung diseases su

144 chronic inflammation, mucus hypersecretion, airway remodeling, emphysema, and reduced lung function.

145 Thoracic imaging provides a way to quantify airway remodeling, emphysematous destruction, regional v

146 re-COPD already show fewer small airways and airway remodeling even in the absence of physiologic air

147 chial T-cell and eosinophil accumulation and airway-remodeling features, such as goblet cell hyperpla

148 d airway remodeling, mice that had developed airway remodeling following 3 mo of repetitive OVA chall

149 the respiratory epithelium and the degree of airway remodeling following alloimmune injury.

150 ow that ablation of TRPC1 in mice alleviates airway remodeling following house dust mite (HDM) challe

151 ASM cell growth and migration that occur in airway remodeling found in asthma and chronic obstructiv

152 this deficit occurs first or is secondary to airway remodeling has been unclear.

153 way inflammation/hyperreactivity and chronic airway remodeling/hyperreactivity phenotypes (the latter

154 To determine the role of IL-5 in airway remodeling, IL-5-deficient and WT mice were sensi

155 way hyperresponsiveness in 4 wk, followed by airway remodeling in 8 wk.

156 dy goal was to determine whether established airway remodeling in a mouse asthma model is reversible

157 eculate that this response may contribute to airway remodeling in allergic inflammation.

158 mmunity; and the development of fibrosis and airway remodeling in animal models of lung injury and al

159 onchiolar fibrosis is a prominent feature of airway remodeling in asthma and involves fibroblast grow

160 nse and indicate that factor Xa functions in airway remodeling in asthma by stimulating mucin product

161 ssment of the ECM, and the data suggest that airway remodeling in asthma involves the progressive acc

162 However, the contribution of ETS to airway remodeling in asthma is at present unknown.

163 Airway remodeling in asthma is defined by several struct

164 ooth muscle (ASM) is an important feature of airway remodeling in asthma that is characterized by enh

165 tion-selective ERK1/2 inhibitors to mitigate airway remodeling in asthma with defined regulation of E

166 e marrow-derived fibroblasts are involved in airway remodeling in asthma, but the role and mechanism

167 The ATF6 target gene SERCA2b, implicated in airway remodeling in asthma, was strongly induced in the

168 x, and vascularity are prominent features of airway remodeling in asthma, whereas the extent of such

169 a T-helper 2 cytokine, is a key mediator of airway remodeling in asthma, yet the mechanism through w

170 ellular matrix (ECM) changes associated with airway remodeling in asthma, yet they provide no informa

171 rtant mechanism postulated to play a role in airway remodeling in asthma.

172 they may play a role in the pathogenesis of airway remodeling in asthma.

173 el FABP4 as a potential target of pathologic airway remodeling in asthma.

174 ion of SERCA2b, which has been implicated in airway remodeling in asthma.

175 e-9 is implicated in airway inflammation and airway remodeling in asthma.

176 and goblet cell hyperplasia consistent with airway remodeling in asthma.

177 ersistent symptoms but may reduce aspects of airway remodeling in asthma.

178 hypertrophy and hyperplasia, contributing to airway remodeling in asthma.

179 IL-13 is a key cytokine involved in airway remodeling in asthma.

180 ed in the pursuit of therapeutic options for airway remodeling in asthma.

181 ration and migration are major components of airway remodeling in asthma.

182 fibronectin are major pathologic features of airway remodeling in asthma.

183 actor Ets-1, and suggest a role for Ets-1 in airway remodeling in asthma.

184 jor regulators of ASM cell proliferation and airway remodeling in asthma.

185 They may be effective in reducing airway remodeling in asthma.

186 tribute to the initiation and progression of airway remodeling in asthmatic patients by recruiting fi

187 fore might contribute to the pathogenesis of airway remodeling in asthmatic patients.

188 argeting PVT1 might be effective in reducing airway remodeling in asthmatic patients.

189 tory cell migration, DP2 might contribute to airway remodeling in asthmatic patients.

190 TGF-beta1 is thought to play a role in airway remodeling in asthmatic subjects.

191 mediate the effects of TGF-beta1 and promote airway remodeling in children with severe asthma.

192 PAR2 prevents allergic inflammation, AHR and airway remodeling in chronic allergic airway inflammatio

193 he current literature emphasizes the role of airway remodeling in chronic persistent asthma and its p

194 There is a lack of proximal airway remodeling in cluster 2 subjects.

195 ing glucose metabolism, thus contributing to airway remodeling in COPD pathogenesis.

196 abnormalities, gas trapping, emphysema, and airway remodeling in COPD.

197 tion and likely the cellular basis of distal airway remodeling in COPD.

198 duction in peripheral blood eosinophilia and airway remodeling in CpG-ODN-treated mice emphasized its

199 esis of these alterations, the importance of airway remodeling in generating the asthma phenotype, an

200 ogic analysis of the lung showed evidence of airway remodeling in mice exposed to HDM, with goblet ce

201 the impact of early biological treatment on airway remodeling in patients with moderate-to-severe as

202 scle (ASM) mass is an essential component of airway remodeling in patients with severe asthma, yet th

203 tudy to evaluate the effect of gallopamil on airway remodeling in patients with severe asthma.

204 ely steroid-resistant mediator that promotes airway remodeling in patients with STRA and is an import

205 vestigate the relationship between IL-33 and airway remodeling in pediatric patients with STRA.

206 trate an enhanced risk of emphysema or small airway remodeling in response to cigarette smoke.

207 Although airway remodeling in severe and/or fatal asthma is still

208 scle (BSM) mass, a characteristic feature of airway remodeling in severe asthma, is associated with r

209 Conclusions: IL-13 drives features of airway remodeling in severe asthma, which are partially

210 uscle hypertrophy is one of the hallmarks of airway remodeling in severe asthma.

211 Studies of allergen induced airway remodeling in transgenic mice suggest an importan

212 ntial clinical application of NLOM to assess airway remodeling in vivo.

213 The higher degree of airway remodeling in WT mice was associated with higher

214 icantly increases levels of allergen-induced airway remodeling (in particular smooth muscle thickness

215 nophilic airway inflammation and features of airway remodeling, in particular subepithelial fibrosis,

216 Important pathologic components of airway remodeling include fibrosis and abnormal innate a

217 y epithelial damage and hyperreactivity, and airway remodeling including smooth muscle hyperplasia an

218 TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracel

219 ys a central role in bronchoconstriction and airway remodeling, including airway smooth muscle growth

220 tracts induced a severe phenotype of chronic airway remodeling, including exacerbated mucus productio

221 siveness and reduced several key features of airway remodeling, including goblet cell hyperplasia and

222 mice have significantly increased levels of airway remodeling, including increased airway smooth mus

223 nes in airway epithelium in allergen-induced airway remodeling, including peribronchial fibrosis and

224 hat computed tomographic (CT) measurement of airway remodeling instead of emphysema may correlate wit

225 ion of the potential effects of biologics on airway remodeling into three temporal effects: early eff

226 Airway remodeling is a critical hallmark of chronic asth

227 Airway remodeling is a detrimental and refractory proces

228 Airway remodeling is a prominent feature of asthma, whic

229 Airway remodeling is a prominent feature of certain immu

230 Airway remodeling is a prominent pathologic feature in p

231 Chronic airway remodeling is a serious consequence of asthma, wh

232 Airway remodeling is a structural change involving the d

233 Asthma airway remodeling is linked to Th2 inflammation.

234 mice had significantly increased markers of airway remodeling like collagen deposition.

235 with features of type 2 immune responses and airway remodeling like those seen in mice with global de

236 rs only a single airway level in summarizing airway remodeling, limiting its accuracy.

237 thus, mechanisms other than inflammation and airway remodeling may be involved in the pathogenesis of

238 Thus, pathways leading to certain aspects of airway remodeling may not depend on leukocyte recruitmen

239 ing YKL-40 levels (r=0.55, P<0.001) and with airway remodeling (measured as the thickness of the sube

240 quences of DNA (ISS) can reverse established airway remodeling, mice that had developed airway remode

241 Airway remodeling might explain lung function decline am

242 Baseline qCT measures of more severe airway remodeling, more small airway disease and hyperin

243 Naphthalene-induced airway remodeling nonsignificantly increased the number

244 t that PAI-1 could play an important role in airway remodeling of asthma, and inhibition of PAI-1 act

245 increased airway smooth muscle mass seen in airway remodeling of patients with severe asthma.

246 of life caused alveolar enlargement without airway remodeling or peribronchiolar nodules.

247 ignificant eosinophilic airway inflammation, airway remodeling, or increased airway hyperreactivity t

248 e dependent (large alveoli) and independent (airway remodeling, peribronchiolar nodules) of lung grow

249 role for altered ECM production in asthmatic airway remodeling, possibly regulated by unbalanced AEC

250 is a key determinant in the control of lower airway remodeling posttransplantation.

251 at ORMDL3 plays an important role in vivo in airway remodeling potentially through ATF6 target genes

252 Increased levels of airway remodeling preceded increased levels of airway in

253 the magnitude of airway hyperreactivity and airways remodeling produced in nonhuman primates with ex

254 lantation is characterized by fibrotic small airway remodeling, recognizable on high-resolution compu

255 airway inflammation, the exact mechanism of airway remodeling remains largely unknown.

256 -kappaB in allergen-induced inflammation and airway remodeling remains unclear.

257 satile functions, the role of Lyn in chronic airway remodeling remains undefined.

258 ossesses versatile functions but its role in airway remodeling remains undefined.

259 asthma phenotype, and the natural history of airway remodeling responses have not been adequately def

260 rate that CCR1 is a major contributor to the airway remodeling responses that arise from A. fumigatus

261 ining the reversibility of transgene-induced airway remodeling responses.

262 terleukin 11 (IL-11) and IL-13 might make to airway remodeling responses.

263 s associated with eosinophil recruitment and airway remodeling revealed that levels of eotaxin-1, IL-

264 c phenotype (airways hyperresponsiveness and airways remodeling), rhesus monkeys with experimentally

265 to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in

266 provide new therapeutic approaches to alter airway remodeling seen in patients with chronic airflow

267 mice that had already developed established airway remodeling significantly reduced the degree of ai

268 rmine the role of Smad 3 in allergen-induced airway remodeling, Smad 3-deficient and wild-type (WT) m

269 evels of expression of genes associated with airway remodeling (TGF-beta1, ADAM8) were detected in ai

270 reased expression of genes important to both airway remodeling [TGF-beta1, 5-lipoxygenase (5-LO)] and

271 re to OVA allergen induces greater levels of airway remodeling than exposure to either chronic ETS or

272 smooth muscle (BSM) mass is a key feature of airway remodeling that classically distinguishes severe

273 The irreversible airway remodeling that occurs in asthma has been attribu

274 the adaptive immune system is essential for airway remodeling that occurs in mice that are chronical

275 tissues from asthmatic subjects with severe airway remodeling that was similar to that seen in the I

276 ) signaling, PDGF- and angiotensin-regulated airway remodeling, the JAK-STAT signaling pathway, and i

277 heir importance is unknown in the context of airway remodeling, their involvement in atherosclerosis

278 have used a mouse model of allergen-induced airway remodeling to determine whether the combination o

279 a wide range of studies, including those on airway remodeling, transepithelial transport and inflamm

280 evaluated as markers of activation of upper airway remodeling using image analysis, together with re

281 4 regulates Dermatophagoides farinae-induced airway remodeling via 2 distinct pathways modulating mat

282 t Gal-3 is an important lectin that promotes airway remodeling via airway recruitment of inflammatory

283 resistance, airway hyperreactivity, and also airway remodeling via effects on other cell types includ

284 identify TRPC1 as a modulator of HDM-induced airway remodeling via STAT3-mediated increase in mucus p

285 Airway remodeling was analyzed at baseline and after tre

286 Airway remodeling was assessed in Hhip(+/-) and Hhip(+/-

287 This increased airway remodeling was associated with selective activati

288 Airway remodeling was measured by using histology, colla

289 Moreover, airway remodeling was significantly increased in allergi

290 irway inflammation, hyperresponsiveness, and airway remodeling were analyzed in allergen-sensitized a

291 Vascular and airway remodeling, which are characterized by airway smo

292 Prolonged inflammation may lead to airway remodeling, which can result in physiologic abnor

293 xious environmental stimuli that can trigger airway remodeling, which contributes significantly to ai

294 mechanisms responsible for the initiation of airway remodeling, which contributes to decreased lung f

295 ta3 isoform and modulates the development of airway remodeling, which may have therapeutic implicatio

296 nd T cell-predominant inflammatory response, airway remodeling with increased types III and I collage

297 Airway remodeling with progressive epithelial alteration

298 mononuclear cell infiltrates and impressive airways remodeling with subepithelial fibrosis.

299 HR and a significant spontaneous increase in airway remodeling, with increased smooth muscle mass and

300 hma is previously unknown, regulates AHR and airway remodeling without airway inflammation through a