ライフサイエンスコーパス: lung fibrosis

1 Endothelial cells are an integral part in lung fibrosis.

2 ical TGF-beta1/SMAD3 signaling that promotes lung fibrosis.

3 turation was sufficient to protect mice from lung fibrosis.

4 SPP1 levels contribute to sex differences in lung fibrosis.

5 alterations in the lung tissue which lead to lung fibrosis.

6 gainst bleomycin injury-induced experimental lung fibrosis.

7 eptors (C3aR and C5aR) in the progression of lung fibrosis.

8 it plays a similar role in radiation-induced lung fibrosis.

9 minish in association with the resolution of lung fibrosis.

10 broblast phenotype and mediates experimental lung fibrosis.

11 vascular niche regulates alveolar repair and lung fibrosis.

12 rations in regulatory T cells can exacerbate lung fibrosis.

13 ness could lead to therapeutic approaches in lung fibrosis.

14 in neurodegeneration, cancer, and liver and lung fibrosis.

15 ffers a novel anti-fibrotic strategy against lung fibrosis.

16 ver, this unexpectedly led to an increase in lung fibrosis.

17 macrophage migration and enhances mammalian lung fibrosis.

18 macrophage migration and enhances mammalian lung fibrosis.

19 ignal through STAT-3, may also contribute to lung fibrosis.

20 Chronic HP may evolve to lung fibrosis.

21 ed AEC proliferation and protected mice from lung fibrosis.

22 e vulnerable to apoptosis and development of lung fibrosis.

23 F-A (Mkl1)-deficient mice are protected from lung fibrosis.

24 njections of Slit2 inhibit bleomycin-induced lung fibrosis.

25 tion and timing of Wnt pathway inhibitors in lung fibrosis.

26 ration of myofibroblasts and/or experimental lung fibrosis.

27 have been implicated in the pathogenesis of lung fibrosis.

28 CD4+CD25+FoxP3+ in TGF-beta1-induced murine lung fibrosis.

29 recognized as important causes of inherited lung fibrosis.

30 profibrotic MMP-8 during bleomycin-mediated lung fibrosis.

31 fibroblast interaction in the progression of lung fibrosis.

32 ogressing IPF and a mouse bleomycin model of lung fibrosis.

33 ulation and in the murine bleomycin model of lung fibrosis.

34 and these mice are resistant to experimental lung fibrosis.

35 eedback loop between miR-17~92 and DNMT-1 in lung fibrosis.

36 tributors to the myofibroblast population in lung fibrosis.

37 alveolar epithelium during bleomycin-induced lung fibrosis.

38 have greater lung inflammation, but reduced lung fibrosis.

39 ion of Mkl1 protected mice from experimental lung fibrosis.

40 ys a key role in limiting the development of lung fibrosis.

41 CT (HRCT) abnormalities and serum markers of lung fibrosis.

42 could attenuate development of experimental lung fibrosis.

43 factors as potential therapeutic targets in lung fibrosis.

44 lated in the lungs of mice with experimental lung fibrosis.

45 s to be an important contributory process to lung fibrosis.

46 ays an important role in the pathogenesis of lung fibrosis.

47 ant role in mediating the ventilator-induced lung fibrosis.

48 op new therapeutic strategies for preventing lung fibrosis.

49 ition in well-characterized murine models of lung fibrosis.

50 eral metalloprotease genes and an absence of lung fibrosis.

51 cumulation, and inhibited the development of lung fibrosis.

52 ysfunction as a trigger of ROS-formation and lung fibrosis.

53 0) and develop more severe bleomycin-induced lung fibrosis.

54 dministration of recombinant IL-22 inhibited lung fibrosis.

55 tudies lend insight into the pathogenesis of lung fibrosis.

56 ministration is limited by bleomycin-induced lung fibrosis.

57 lung fibroblast expression of Thy-1 prevents lung fibrosis.

58 hR) or inhibiting AhR signaling, accelerated lung fibrosis.

59 disease, particularly in cases of idiopathic lung fibrosis.

60 g fibroblasts and mesenchymal cells and more lung fibrosis.

61 h murine gammaherpesvirus 68 (MHV68) develop lung fibrosis.

62 broblast differentiation is a key feature of lung fibrosis.

63 role in myofibroblast differentiation during lung fibrosis.

64 These knockout mice also showed impaired lung fibrosis.

65 by CD4(+) T cell alveolitis and progressive lung fibrosis.

66 ntioxidant enzyme, inhibits inflammation and lung fibrosis.

67 oblasts represents a hallmark of progressive lung fibrosis.

68 ifests as progressive airway and parenchymal lung fibrosis.

69 in AEC2 cells exacerbates bleomycin-induced lung fibrosis.

70 ic population using agents designed to treat lung fibrosis.

71 carbon monoxide (CO) abrogates experimental lung fibrosis.

72 of LOXL3, an emerging therapeutic target for lung fibrosis.

73 ibrotic lung disease and in murine models of lung fibrosis.

74 lready shown to be effective in experimental lung fibrosis.

75 5 weeks later, indicating protection against lung fibrosis.

76 strating the importance of mTOR signaling in lung fibrosis.

77 -17B (IL-17B) during bleomycin-induced mouse lung fibrosis.

78 ty and mortality associated with spontaneous lung fibrosis.

79 ne suppression for the treatment of skin and lung fibrosis.

80 n mediating AEC mtDNA damage, apoptosis, and lung fibrosis.

81 se, followed by damage to alveolar cells and lung fibrosis.

82 that the blockade of C' receptors mitigates lung fibrosis.

83 brosis in the experimental models of PAH and lung fibrosis.

84 ut mice exhibited enhanced bleomycin-induced lung fibrosis.

85 17A is a potential mechanism in ameliorating lung fibrosis.

86 a TH mimetic, also blunted bleomycin-induced lung fibrosis.

87 ctive form of AOC3, were also protected from lung fibrosis.

88 eomycin-induced complement activation during lung fibrosis.

89 sure is one important environmental cause of lung fibrosis.

90 the myeloid compartment in radiation-induced lung fibrosis.

91 e-resident macrophages in the development of lung fibrosis.

92 gated the role of IL-17A in regulating C' in lung fibrosis.

93 ion of myofibroblasts and the development of lung fibrosis.

94 also significantly reduced radiation-induced lung fibrosis.

95 Asbestos- or bleomycin-induced lung fibrosis, AEC mtDNA damage, and apoptosis in wild-t

96 quences of lymphatic remodeling in mice with lung fibrosis after bleomycin injury or telomere dysfunc

97 s or disruption of TBX4 signaling attenuated lung fibrosis after bleomycin-induced injury.

98 and attenuated the late-stage progression of lung fibrosis after bleomycin.

99 7A modestly decreased airway and parenchymal lung fibrosis, along with a striking reduction in pulmon

100 the contribution of the microenvironment to lung fibrosis and adenocarcinoma progression, two pathol

101 BLM in chemotherapy, which can progress into lung fibrosis and affect up to 46% of the total patient

102 expressing bone marrow-derived cells induce lung fibrosis and alter the production of T-cell mediato

103 Exposure to silica can cause lung fibrosis and cancer.

104 ed an aggressive phenotype leading to severe lung fibrosis and death after bleomycin-induced injury.

105 c and a therapeutic target in SSc-associated lung fibrosis and demonstrate that Chit1 augments TGF-be

106 Furthermore, lung fibrosis and EndoMT responses were reduced in VEC-m

107 or in vivo analysis, we used mouse models of lung fibrosis and fibrotic human lung tissue.

108 in mice with established AdTGF-beta1-induced lung fibrosis and further increased in mice with pneumoc

109 ACE significantly reduced bleomycin-induced lung fibrosis and implicates AcSDKP in the mechanism of

110 the mouse lung attenuated bleomycin-induced lung fibrosis and improved lung function.

111 Both in an experimental mouse model of lung fibrosis and in human subjects with idiopathic pulm

112 bronectin was increased in a murine model of lung fibrosis and in human subjects with interstitial lu

113 Inhibition of LXRalpha in experimental lung fibrosis and in IPF lung fibroblasts reduced the ex

114 ing protein- 5 (IGFBP-5) is overexpressed in lung fibrosis and induces the production of extracellula

115 regulator of signaling pathways involved in lung fibrosis and inflammation.

116 ession was up-regulated in bleomycin-induced lung fibrosis and IPF.

117 K1 plays a critical role in the pathology of lung fibrosis and is a novel therapeutic target.

118 ll add new insights into the pathogenesis of lung fibrosis and may lead to new therapeutic approaches

119 ese studies support a function for CD44V6 in lung fibrosis and offer proof of concept for therapeutic

120 -fold decrease in hyaluronan, both linked to lung fibrosis and PH, were also observed.

121 plays an active role in the pathogenesis of lung fibrosis and PH.

122 fies galectin-3 as an important regulator of lung fibrosis and provides a proof of principle for gale

123 ce and progression of complications, such as lung fibrosis and pulmonary arterial hypertension.

124 SFTPC-expressing mice developed exaggerated lung fibrosis and reduced static lung compliance compare

125 hronic inhalation of silica particles causes lung fibrosis and silicosis.

126 the SRF/MRTF pathway in the pathobiology of lung fibrosis and suggest that its inhibition can help r

127 hat STAT-3 contributes to the development of lung fibrosis and suggest that STAT-3 may be a therapeut

128 ary fibrosis and strengthen the link between lung fibrosis and telomere dysfunction.

129 2 in fibroblasts are protected from skin and lung fibrosis and that a disintegrin and metalloproteina

130 However, whether HSM may be used to prevent lung fibrosis and the mechanism underlying this activity

131 plays a critical role in the development of lung fibrosis and the signaling involved may present a n

132 Lung fibrosis and tissue remodeling are features of chro

133 ered a critical event in the pathogenesis of lung fibrosis and tumor metastasis.

134 CXCL4 levels correlated with skin and lung fibrosis and with pulmonary arterial hypertension.

135 show 1) a critical role for ER and let-7 in lung fibrosis, and 2) that IGF may stimulate ER in an E(

136 king tenascin-C show attenuation of skin and lung fibrosis, and accelerated fibrosis resolution.

137 rome, chronic obstructive pulmonary disease, lung fibrosis, and blunted lung development associated w

138 Mechanical stress induces lung fibrosis, and epithelia-mesenchymal transition may

139 ncreased susceptibility to bleomycin-induced lung fibrosis, and fibroblasts lacking Id1 exhibited enh

140 enin-angiotensin system is a key mediator of lung fibrosis, and its pro-fibrotic effect is independen

141 improved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches w

142 established chronic GVHD reversed liver and lung fibrosis, and pulmonary dysfunction characteristic

143 sion of type I collagen in bleomycin-induced lung fibrosis, and to delineate the mechanisms of action

144 ch as systemic sclerosis; kidney, liver, and lung fibrosis; and the stromal reaction to certain epith

145 Among the most common forms of lung fibrosis are idiopathic pulmonary fibrosis (IPF) an

146 ncreased numbers of fibroblasts and enhanced lung fibrosis as determined by semiquantitative histolog

147 Mortality correlated with extent of lung fibrosis as SMR increased from 2.2 with no fibrosis

148 Skin and lung fibrosis as well as immunological features were stu

149 d high-resolution imaging modality to detect lung fibrosis at early stage and to monitor disease prog

150 nd contributes to diseases such as liver and lung fibrosis, atherosclerosis, diabetes and osteoarthri

151 in fibrotic mice arrested the progression of lung fibrosis, attenuated cellular apoptosis (caspase-3/

152 rates correlated with presence or absence of lung fibrosis, being 83% and 80%, respectively, with no

153 ering with DNM3OS function not only prevents lung fibrosis but also improves established pulmonary fi

154 eta-catenin signaling has been implicated in lung fibrosis, but how this occurs and whether expressio

155 These cells are thought to facilitate lung fibrosis, but the exact mechanisms of their profibr

156 sminogen activation to plasmin protects from lung fibrosis, but the mechanism underlying this antifib

157 sted whether ER stress causes or exacerbates lung fibrosis by (i) conditional expression of a mutant

158 a1 induces myofibroblast differentiation and lung fibrosis by activation of the reactive oxygen speci

159 SIRT3 deficiency promotes lung fibrosis by augmenting alveolar epithelial cell mit

160 growth factor-beta-signalling and prevented lung fibrosis by decreasing the stability of Smad3 in an

161 suggest that its inhibition can help resolve lung fibrosis by promoting fibroblast apoptosis.

162 ng acute inflammatory response, but promotes lung fibrosis by reducing lung levels of IP-10 and MIP-1

163 c pulmonary symbiotic commensals can promote lung fibrosis by regulating a profibrotic inflammatory c

164 acts as an endogenous negative regulator of lung fibrosis by repressing multiple profibrotic respons

165 ects were assessed in the bleomycin model of lung fibrosis by SHP2-lentiviral administration and tran

166 n of LR-MSC and attenuates bleomycin-induced lung fibrosis by targeting Smad7.

167 We investigated the role of C3aR and C5aR in lung fibrosis by using bleomycin-injured mice with fibro

168 s in humans with IPF and in a mouse model of lung fibrosis caused by lung-targeted, transgenic overex

169 In the bleomycin (BLM) model of lung fibrosis, CKO mice had reduced fibrosis, lesser fib

170 iSP-D mice off Dox (SP-D off) had increased lung fibrosis compared with mice on Dox (SP-D on).

171 expansion in wild-type mice with established lung fibrosis completely inhibited pneumococcal infectio

172 models of lung injury and persists in human lung fibrosis, creating a distinct cell-cell communicati

173 of mitochondrial fusion in AEC2 function and lung fibrosis development remains unknown.

174 ncept for therapeutic targeting of CD44V6 in lung fibrosis disorders.

175 stration of AcSDKP to wild-type mice reduced lung fibrosis due to bleomycin administration.

176 Mice with lung fibrosis due to telomere dysfunction and humans wit

177 rities include develop newer models of human lung fibrosis, engage current and new stakeholders to pr

178 in mice with pneumococcal infection-induced lung fibrosis exacerbation.

179 on of integrin and Src kinase interaction to lung fibrosis has not been mechanistically investigated.

180 ry and oncologic indications, their roles in lung fibrosis have not been comprehensively assessed.

181 and lung inflammation, and bleomycin-induced lung fibrosis; however, the cellular source of COX-2 tha

182 of FRNK function in vivo leads to increased lung fibrosis in an experimental mouse model.

183 es enhanced Itgb6 expression and exaggerated lung fibrosis in an in vivo model of fibrosis, whereas t

184 LC(20) phosphorylation and bleomycin-induced lung fibrosis in both relaxin knockout and wild-type mic

185 n, we find increased mortality and increased lung fibrosis in FAP-deficient mice compared with wild-t

186 eubiquitinase CYLD led to the development of lung fibrosis in mice after infection with Streptococcus

187 Wnt coreceptor, Lrp5, is a genetic driver of lung fibrosis in mice and a marker of disease progressio

188 ofibroblast contraction in bleomycin-induced lung fibrosis in mice and in fibroblastic foci of human

189 stimulation and in driving the induction of lung fibrosis in mice in response to bleomycin challenge

190 nally regulated BMPER expression and reduced lung fibrosis in mice in vivo.

191 ent with a blocking antibody to CD44 reduced lung fibrosis in mice in vivo.

192 d its contribution to experimentally induced lung fibrosis in mice, and defined the mechanism for our

193 uppressing infection-induced exacerbation of lung fibrosis in mice, and their expansion may offer a n

194 obes diminished the severity of experimental lung fibrosis in mice, even when treatment was started 5

195 n signaling and attenuates bleomycin-induced lung fibrosis in mice, while concurrently preserving the

196 of IPF LFs and attenuates bleomycin-induced lung fibrosis in mice.

197 administration of human syndecan-2 abrogated lung fibrosis in mice.

198 roduction of miR-31 ameliorated experimental lung fibrosis in mice.

199 ogeneity of macrophages in bleomycin-induced lung fibrosis in mice.

200 on stimulated by PDGF-BB and reduced in vivo lung fibrosis in mice.

201 evels in bronchoalveolar lavage and prevents lung fibrosis in mice.

202 Surprisingly, the reduction in liver and lung fibrosis in MMP12-deficient mice was not associated

203 MAP3K19 was required for the development of lung fibrosis in SCID mice humanized with IPF lung fibro

204 tered intratracheally attenuated BLM-induced lung fibrosis in SP-D(-/-) mice.

205 ilica are associated with the development of lung fibrosis in the forms of asbestosis and silicosis,

206 prevents excessive inflammation and eventual lung fibrosis in this murine model of B. subtilis-induce

207 f therapeutically administered CCG-203971 on lung fibrosis in two distinct murine models of fibrosis

208 te myofibroblast function in vitro and limit lung fibrosis in vivo.

209 Bleomycin-induced lung fibrosis in wild-type and miR-155(-/-) mice was ana

210 molecule (CWHM 12) attenuated both liver and lung fibrosis, including in a therapeutic manner.

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

212 Of note, lung fibrosis induced after intratracheal bleomycin chal

213 utic dosing regimen substantially attenuated lung fibrosis induced by bleomycin in C57BL/6 mice.

214 loss of the Wnt coreceptor Lrp5 in models of lung fibrosis induced by bleomycin or an adenovirus enco

215 a, Lrp5 null mice were not protected against lung fibrosis induced by TGF-beta.

216 n fibrotic lung disease, and create a global lung fibrosis initiative that unites these multifaceted

217 protective effects of GRN510 against induced lung fibrosis involves specific types of lung cells.

218 Lung fibrosis is an unabated wound healing response char

219 levels, demonstrated that the resolution of lung fibrosis is blocked by the failure of adenosine lev

220 The increase in lung fibrosis is confirmed at the histological, biochemi

221 extent to which STAT-3 inhibition decreases lung fibrosis is investigated.

222 late TGF-beta/BMP signaling, but its role in lung fibrosis is not clear.

223 However, the role of miRNAs in lung fibrosis is not well characterized.

224 e preclinical natural history of progressive lung fibrosis is poorly understood.Objectives: Our goals

225 Lung fibrosis is the hallmark of the interstitial lung d

226 sis during stress responses, but its role in lung fibrosis is unknown.

227 onary function and physical health, although lung fibrosis is visibly unaltered.

228 MT/MET to embryogenesis, renal fibrosis, and lung fibrosis is well documented, role of EMT/MET in liv

229 The increase in lung fibrosis led to a substantial decrease in respirato

230 In a murine model of lung fibrosis, levels of all three oxidative tyrosine mo

231 In a mouse model of bleomycin-induced lung fibrosis, Lonidamine reduced the expression of gene

232 ty of AOC3 contributes to the development of lung fibrosis mainly by regulating the accumulation of p

233 , which, when aberrantly high, contribute to lung fibrosis, maladaptive vascular remodeling, and alle

234 t advances in the treatment of some forms of lung fibrosis, many gaps in knowledge about natural hist

235 This is because many disorders resulting in lung fibrosis may be similar in their initial clinical a

236 In a bleomycin-induced lung fibrosis model we used wild-type MMTV mice and a tr

237 In the murine bleomycin-induced lung fibrosis model, GSK3008348 engages alphavbeta6, ind

238 Using an in vivo bleomycin-induced lung fibrosis model, we reveal a clock "gated" pulmonary

239 Lung fibrosis models and cell culture systems were emplo

240 In vivo lung fibrosis models and ex vivo cell culture systems we

241 ibrotic responses in bleomycin (BLM) induced lung fibrosis models.

242 ft models of cancer, as well as in liver and lung fibrosis models.

243 nd TGF-beta secretion in a bleomycin-induced lung fibrosis mouse model that was accompanied by reduce

244 Lung fibrosis occurs in ~80% of patients with SSc; 25% t

245 1 PET radiotracer may be useful for studying lung fibrosis or for developing LPA1-targeting drugs.

246 ounced fatigue and are at risk of developing lung fibrosis or irreversible damage to other organs.

247 vely, were injected with bleomycin to induce lung fibrosis (or saline as control), and the extracted

248 hibited significantly less radiation-induced lung fibrosis (P < 0.010).

249 fibrosis and 69% and 56%, respectively, with lung fibrosis (P = 0.03).Conclusions: The mere presence

250 We propose that in lung fibrosis, perturbed molecular checkpoints on the wa

251 monary fibrosis, a fatal form of progressive lung fibrosis, previous work has shown that loss of Thy-

252 uate fibrotic processes and so contribute to lung fibrosis progression.

253 However, the functions of MCs in lung fibrosis remain largely unknown.

254 unction of endothelial miR-155 and SHIP-1 in lung fibrosis remain unknown.

255 there are significant gaps in understanding lung fibrosis resolution, accelerated improvements in bi

256 Radiation-induced lung fibrosis (RILF) is a common side effect for patient

257 icacy in a murine model of bleomycin-induced lung fibrosis similar to that of a known nonselective ga

258 Furthermore, the STING mutant mice developed lung fibrosis similar to that of patients with SAVI.

259 jection, S-17092-treated N-KO mice developed lung fibrosis similar to wild-type mice.

260 lymphotoxin beta receptor (LTbetaR) reduces lung fibrosis, smooth muscle hyperplasia and airway hype

261 Unit density distributions and selected for lung fibrosis staging.

262 all, preclinical studies in animal models of lung fibrosis suggest that MSCs might be effective in th

263 AF2ERKI mice developed BLM-induced lung fibrosis, suggesting a role for growth factors in s

264 rate that CD73 potentiates radiation-induced lung fibrosis, suggesting that existing pharmacologic st

265 ency is protective against bleomycin-induced lung fibrosis, suggesting that miR-145 may be a potentia

266 ed SSc as well as in sera from patients with lung fibrosis suggests that IFNalpha may contribute to t

267 erative and proliferative disease, including lung fibrosis (surfactant protein C precursor; pro-SP-C)

268 le mice are more sensitive to silica-induced lung fibrosis than silica-treated female mice.

269 ese mice developed more robust granulomatous lung fibrosis than wild-type counterparts.

270 any reports about pulmonary blood vessels in lung fibrosis, the contribution of lymphatics to fibrosi

271 ified genes that are known to be involved in lung fibrosis, the inflammatory response of cystic fibro

272 of CTGF and demonstrate its contribution to lung fibrosis through transcriptional activation of Col1

273 nti-fibrotic activity in models of liver and lung fibrosis, thus confirming LOXL2 as an important tar

274 vo efficacy in a preclinical animal model of lung fibrosis, thus paving the way for a new treatment o

275 elf-limited bleomycin-induced mouse model of lung fibrosis to a model of persistent fibrosis in an S1

276 dy was to use various models of experimental lung fibrosis to understand when adenosine levels are el

277 ersensitivity pneumonitis that progresses to lung fibrosis upon repeated exposure to the ubiquitous m

278 othesis that SP-D plays an important role in lung fibrosis using a mouse model of fibrosis induced by

279 essed FKBP10 expression in bleomycin-induced lung fibrosis (using quantitative reverse transcriptase-

280 The role of CDH11 in lung fibrosis was determined using the bleomycin model o

281 owth factor (TGF)-beta and bleomycin-induced lung fibrosis was dramatically reduced in mice deficient

282 Bleomycin-induced lung fibrosis was evaluated in Mmp19-deficient and wild-

283 X-box binding protein 1 (XBP1) mRNA, but no lung fibrosis was identified in the absence of a second

284 Rat lung fibrosis was induced using transient gene expressio

285 Histologic evidence of lung fibrosis was observed by 25 weeks after irradiation

286 argeted epithelial insult and contributes to lung fibrosis, we administered diphtheria toxin to trans

287 +) gammadelta T cells in B. subtilis-induced lung fibrosis, we exposed transgenic Vgamma6/Vdelta1 mic

288 Extent of ground glass opacity and lung fibrosis were assessed visually.

289 ar lavage and the lung, as well as levels of lung fibrosis, were reduced 7 d after intranasal deliver

290 AT overexpression reduced several indices of lung fibrosis, whereas down-regulation of native LYCAT e

291 in expression in mice with bleomycin-induced lung fibrosis, whereas it had no effect on basal levels

292 er their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macropha

293 Its induction in mice drives lung fibrosis, which is abrogated by administration of a

294 3% of patients with SSc and are a marker for lung fibrosis, which is often severe.

295 e and negative cohorts was the prevalence of lung fibrosis, which occurred in 79% of the anti-U11/U12

296 ant restored pulmonary function and reversed lung fibrosis, which was associated with reduced macroph

297 y fibrosis (IPF) is a disease of progressive lung fibrosis with a high mortality rate.

298 pulmonary fibrosis (IPF) is a severe form of lung fibrosis with a high mortality rate.

299 t may also promote dermal, heart, liver, and lung fibrosis with repetitive signaling under defined ci

300 iveness of slowing the progression of murine lung fibrosis with the IGF-1R inhibitor OSI-906.