ライフサイエンスコーパス: lung fibrosis

1 e vulnerable to apoptosis and development of lung fibrosis.

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

3 njections of Slit2 inhibit bleomycin-induced lung fibrosis.

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

5 ration of myofibroblasts and/or experimental lung fibrosis.

6 have been implicated in the pathogenesis of lung fibrosis.

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

8 recognized as important causes of inherited lung fibrosis.

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

10 fibroblast interaction in the progression of lung fibrosis.

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

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

13 and these mice are resistant to experimental lung fibrosis.

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

15 tributors to the myofibroblast population in lung fibrosis.

16 alveolar epithelium during bleomycin-induced lung fibrosis.

17 have greater lung inflammation, but reduced lung fibrosis.

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

19 ion of Mkl1 protected mice from experimental lung fibrosis.

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

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

22 could attenuate development of experimental lung fibrosis.

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

24 factors as potential therapeutic targets in lung fibrosis.

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

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

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

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

29 op new therapeutic strategies for preventing lung fibrosis.

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

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

32 eral metalloprotease genes and an absence of lung fibrosis.

33 cumulation, and inhibited the development of lung fibrosis.

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

35 dministration of recombinant IL-22 inhibited lung fibrosis.

36 tudies lend insight into the pathogenesis of lung fibrosis.

37 ministration is limited by bleomycin-induced lung fibrosis.

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

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

40 disease, particularly in cases of idiopathic lung fibrosis.

41 ut mice exhibited enhanced bleomycin-induced lung fibrosis.

42 g fibroblasts and mesenchymal cells and more lung fibrosis.

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

44 broblast differentiation is a key feature of lung fibrosis.

45 role in myofibroblast differentiation during lung fibrosis.

46 These knockout mice also showed impaired lung fibrosis.

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

48 ntioxidant enzyme, inhibits inflammation and lung fibrosis.

49 oblasts represents a hallmark of progressive lung fibrosis.

50 nt TGF-beta1 activation in bleomycin-induced lung fibrosis.

51 17A is a potential mechanism in ameliorating lung fibrosis.

52 mice lacking STAT-1 are more susceptible to lung fibrosis.

53 investigate whether T cells are required for lung fibrosis.

54 of differentiation-1 (Id1) in the setting of lung fibrosis.

55 d proteolysis after sciatic nerve injury and lung fibrosis.

56 and collagen deposition in bleomycin-induced lung fibrosis.

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

58 (+/-)) mice in studies of bleomycin-induced lung fibrosis.

59 -13 could play a role in the pathogenesis of lung fibrosis.

60 CR4(+) circulating fibrocytes and attenuated lung fibrosis.

61 icated as a key event in the pathogenesis of lung fibrosis.

62 tream signaling pathways and causes skin and lung fibrosis.

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

64 lpha, and RANTES precede subsequent skin and lung fibrosis.

65 disease, such as tuberculosis, emphysema, or lung fibrosis.

66 a cause of a major clinical problem of HPS, lung fibrosis.

67 eomycin-induced complement activation during lung fibrosis.

68 sure is one important environmental cause of lung fibrosis.

69 the myeloid compartment in radiation-induced lung fibrosis.

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

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

72 ion of myofibroblasts and the development of lung fibrosis.

73 also significantly reduced radiation-induced lung fibrosis.

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

75 turation was sufficient to protect mice from lung fibrosis.

76 SPP1 levels contribute to sex differences in lung fibrosis.

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

78 gainst bleomycin injury-induced experimental lung fibrosis.

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

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

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

82 minish in association with the resolution of lung fibrosis.

83 broblast phenotype and mediates experimental lung fibrosis.

84 vascular niche regulates alveolar repair and lung fibrosis.

85 rations in regulatory T cells can exacerbate lung fibrosis.

86 ness could lead to therapeutic approaches in lung fibrosis.

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

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

89 macrophage migration and enhances mammalian lung fibrosis.

90 macrophage migration and enhances mammalian lung fibrosis.

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

92 Chronic HP may evolve to lung fibrosis.

93 ed AEC proliferation and protected mice from lung fibrosis.

94 uggest dual effects of IL-4 in this model of lung fibrosis: 1) limiting early recruitment of T lympho

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

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

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

98 The rodent bleomycin model of lung fibrosis allows the use of molecular tools to disse

99 n cancers, telomerase activity is induced in lung fibrosis, although its role in this process is unkn

100 subpopulations of fibroblasts contribute to lung fibrosis, although the mechanisms underlying fibrog

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

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

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

104 Exposure to silica can cause lung fibrosis and cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 2 in fibroblasts are protected from skin and lung fibrosis and that a disintegrin and metalloproteina

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

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

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

131 ects the lung in models of bleomycin-induced lung fibrosis and ventilator-induced lung injury.

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

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

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

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

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

137 lial cells (AECs) in bleomycin (BLM)-induced lung fibrosis, and found to induce myofibroblast differe

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

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

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

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

142 scleroderma, with prominent skin thickening, lung fibrosis, and up-regulation of cutaneous collagen m

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

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

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

146 Bleomycin-AG1879 mice are protected from lung fibrosis as evidenced by histopathology, trichrome

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

148 is an important mediator of the interstitial lung fibrosis associated with scleroderma.

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

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

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

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

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

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

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

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

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

158 brosis, we found a significant inhibition of lung fibrosis by imatinib.

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

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

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

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

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

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

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

166 We postulated that lung fibrosis characterized by excessive proliferation o

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

168 Mice with Scl GVHD have skin thickening, lung fibrosis, cutaneous mononuclear cell infiltration,

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

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

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

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

173 the potential role of female sex hormones in lung fibrosis, female rats were ovariectomized and treat

174 -deficient mice showed significantly reduced lung fibrosis following bleomycin (BLM) insult.

175 mice displayed more severe histopathological lung fibrosis, greater accumulation of lung collagen, an

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

177 ution of individual complement components to lung fibrosis has not yet been examined.

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

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

180 Indices of lung fibrosis (hydroxyproline content, collagen accumula

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

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

183 lung, whereas it partially protects against lung fibrosis in an inflammatory profibrotic pulmonary m

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 tor AT1a in the pathogenesis of BLEO-induced lung fibrosis in mice and suggest that AT1 receptor sign

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

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

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

193 n this study, we evaluated bleomycin-induced lung fibrosis in mice with genetic deletion of SFTPC.

194 hypothesized that BLEO-induced apoptosis and lung fibrosis in mice would be inhibited by the AT1 anta

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

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

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

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

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

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

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

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

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

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 sis, we show that OSM is capable of inducing lung fibrosis independently of these pathways.

213 Of note, lung fibrosis induced after intratracheal bleomycin chal

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

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

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

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

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

219 Lung fibrosis is a fatal condition of excess extracellul

220 Lung fibrosis is an unabated wound healing response char

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

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

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

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

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

226 Lung fibrosis is the hallmark of the interstitial lung d

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

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

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

230 e QTL on chromosome 17 for radiation-induced lung fibrosis is within the same region as QTLs identifi

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

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

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

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

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

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

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

238 nded our findings to a rat bleomycin-induced lung fibrosis model, demonstrating a significant decreas

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

240 Lung fibrosis models and cell culture systems were emplo

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

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

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

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

247 distinctly to the development of blm-induced lung fibrosis potentially via their production of differ

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

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

250 lin-1 peptide to mice with bleomycin-induced lung fibrosis reduced fibrosis.

251 ine model of intratracheal bleomycin-induced lung fibrosis, regions of active fibrogenesis demonstrat

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

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

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

255 ight lungs and 75% (12/16) of silicotic left lungs; fibrosis scores > 1 were measured in 91% (10/11)

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

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

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

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

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

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

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

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

264 15 +/- 66 pg/ml) as well as in patients with lung fibrosis than in those without.

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

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

267 ce are more susceptible to bleomycin-induced lung fibrosis than wild-type mice due to 1) enhanced fib

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

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

270 king T cell influx by anti-CD3 Abs abrogated lung fibrosis, thus also implicating T lymphocytes as a

271 e lungs resulted in extension of blm-induced lung fibrosis, thus confirming a role for eosinophils.

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

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

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

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

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

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

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

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

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

281 Lung fibrosis was induced by intratracheal administratio

282 Rat lung fibrosis was induced using transient gene expressio

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

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

285 Thus, to evaluate the role of C5 in lung fibrosis, we compared congenic C5-sufficient and C5

286 the pathogenetic importance of telomerase in lung fibrosis, we examined the effects of telomerase rev

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

288 ering in susceptibility to bleomycin-induced lung fibrosis, we show highly significant linkage to onl

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

290 The same three measures of apoptosis and lung fibrosis were reduced by 89%, 85%, and 75%, respect

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

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

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

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

295 3% of patients with SSc and are a marker for lung fibrosis, which is often severe.

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

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

298 y fibrosis (IPF) is a disease of progressive 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 odels of susceptibility to bleomycin-induced lung fibrosis, with an interaction between Blmpf2 and Bl