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1 ely activated macrophages and contributes to pulmonary fibrosis.
2 case subjects reported no family history of pulmonary fibrosis.
3 en suggested in many disease areas including pulmonary fibrosis.
4 a promising candidate for in vivo imaging of pulmonary fibrosis.
5 understanding of the genetic architecture of pulmonary fibrosis.
6 of a collagen-targeted PET probe for staging pulmonary fibrosis.
7 rotic mechanisms behind Shenks treatment for pulmonary fibrosis.
8 cases of organ fibrosis, such as idiopathic pulmonary fibrosis.
9 D61G/+)) were resistant to bleomycin-induced pulmonary fibrosis.
10 H may thus represent a potential therapy for pulmonary fibrosis.
11 potential therapeutic usefulness of SHP2 in pulmonary fibrosis.
12 cy in knockout mice significantly diminished pulmonary fibrosis.
13 was increased in lung tissues from mice with pulmonary fibrosis.
14 ia involved in a preclinical murine model of pulmonary fibrosis.
15 t that STAT-3 may be a therapeutic target in pulmonary fibrosis.
16 hich are important inflammatory cytokines in pulmonary fibrosis.
17 drives the progression of radiation-induced pulmonary fibrosis.
18 n mouse models of resolvable and progressive pulmonary fibrosis.
19 rrow-derived CD11c(+) cells is essential for pulmonary fibrosis.
20 menon was relevant in vivo in the context of pulmonary fibrosis.
21 trations are elevated early in the course of pulmonary fibrosis.
22 ptors, C3aR and C5aR, to the pathogenesis of pulmonary fibrosis.
23 d both induction of lung AREG expression and pulmonary fibrosis.
24 macrophage apoptosis and were protected from pulmonary fibrosis.
25 lung tissues in a bleomycin-induced model of pulmonary fibrosis.
26 ease such as seen in lung conditions such as pulmonary fibrosis.
27 esigning adenosine based approaches to treat pulmonary fibrosis.
28 ion in the bleomycin-induced murine model of pulmonary fibrosis.
29 -product relationship between LPC and LPA in pulmonary fibrosis.
30 to therapeutically target LPA production in pulmonary fibrosis.
31 nship with disease progression in idiopathic pulmonary fibrosis.
32 play roles in the pathogenesis of idiopathic pulmonary fibrosis.
33 R-MSC) plays an important role in idiopathic pulmonary fibrosis.
34 potential role for Gal-3 in early stages of pulmonary fibrosis.
35 , chronic obstructive pulmonary disease, and pulmonary fibrosis.
36 tidic acid (LPA) is an important mediator of pulmonary fibrosis.
37 rrelated with disease severity of idiopathic pulmonary fibrosis.
38 collagen V overexpression during idiopathic pulmonary fibrosis.
39 e results suggest that SAB potently inhibits pulmonary fibrosis.
40 ofibrogenic cytokines in the pathogenesis of pulmonary fibrosis.
41 Matrix stiffening is a prominent feature of pulmonary fibrosis.
42 nsideration of their use to treat idiopathic pulmonary fibrosis.
43 to develop novel therapies for patients with pulmonary fibrosis.
44 s significantly induced in bleomycin-induced pulmonary fibrosis.
45 activation of TGF-beta1 in rodent and human pulmonary fibrosis.
46 re up-regulated in IPF and bleomycin-induced pulmonary fibrosis.
47 e homeostasis, and alterations can result in pulmonary fibrosis.
48 and in fibroblasts from patients with severe pulmonary fibrosis.
49 the expression of TREM-1 in a mouse model of pulmonary fibrosis.
50 nterstitial lung diseases such as idiopathic pulmonary fibrosis.
51 n alveolar macrophages is directly linked to pulmonary fibrosis.
52 n induce Treg alterations, which can augment pulmonary fibrosis.
53 , leading to the progression of experimental pulmonary fibrosis.
54 ng diseases including asthma, emphysema, and pulmonary fibrosis.
55 obstructive pulmonary disease and idiopathic pulmonary fibrosis.
56 left lung transplantation 8 years prior for pulmonary fibrosis.
57 blast differentiation in the pathogenesis of pulmonary fibrosis.
58 feasibility of clinical trials in idiopathic pulmonary fibrosis.
59 l lung diseases, particularly for idiopathic pulmonary fibrosis.
60 intervenes to offer patients diagnosed with pulmonary fibrosis.
61 e importance of telomere-related pathways in pulmonary fibrosis.
62 ostic and prognostic biomarker of idiopathic pulmonary fibrosis.
63 trials and to guide management of idiopathic pulmonary fibrosis.
64 nd leukocyte recruitment in a mouse model of pulmonary fibrosis.
65 ithelial cell proteinopathy with spontaneous pulmonary fibrosis.
66 are recognized to play a protective role in pulmonary fibrosis.
67 naling has been identified as a regulator of pulmonary fibrosis.
68 tor (PAI-1) are resistant to lung injury and pulmonary fibrosis.
69 nts with IPF and mice with bleomycin-induced pulmonary fibrosis.
70 entiviral delivery blunted bleomycin-induced pulmonary fibrosis.
71 at were deficient in MCU were protected from pulmonary fibrosis.
72 in an early stage when there is only little pulmonary fibrosis.
73 he fibrotic changes that underlie idiopathic pulmonary fibrosis.
74 get that when deregulated enables pathogenic pulmonary fibrosis.
75 e been linked to autosomal-dominant familial pulmonary fibrosis.
76 tions available for patients with idiopathic pulmonary fibrosis.
77 roblasts from human subjects with idiopathic pulmonary fibrosis.
78 blasts, and its contribution to experimental pulmonary fibrosis.
79 nduced in myofibroblasts in human idiopathic pulmonary fibrosis.
80 roRNA and a potential therapeutic target for pulmonary fibrosis.
81 xidase activity regulates the development of pulmonary fibrosis.
82 s congenita, aplastic anemia, and idiopathic pulmonary fibrosis.
83 o as well as in 2 murine treatment models of pulmonary fibrosis, a 3-amino acid point mutant that was
85 indications and diseases, such as idiopathic pulmonary fibrosis, a number may hold promise in the tre
89 to inhibit TGF-beta signalling in idiopathic pulmonary fibrosis, ameliorated BK dysfunction and ASL v
90 tive treatments for patients with idiopathic pulmonary fibrosis, an accurate diagnosis is crucial.
92 me sequence data from 262 case subjects with pulmonary fibrosis and 4,141 control subjects drawn from
93 HOCl developed a diffuse cutaneous SSc with pulmonary fibrosis and anti-DNA topoisomerase 1 autoanti
95 lung biopsies from patients with idiopathic pulmonary fibrosis and bleomycin (BLM)-induced fibrotic
96 ntribute towards diseases such as idiopathic pulmonary fibrosis and chronic obstructive pulmonary dis
97 MT, ATII cells from patients with idiopathic pulmonary fibrosis and chronic obstructive pulmonary dis
99 and collagen deposition in vivo in models of pulmonary fibrosis and collagen-dependent lung cancer me
101 ease progression in patients with idiopathic pulmonary fibrosis and emphysema extent greater than or
104 hway involved in the onset and regulation of pulmonary fibrosis and identify Tc2 cells as key mediato
105 ation in a murine model of radiation-induced pulmonary fibrosis and in idiopathic pulmonary fibrosis,
106 tation significantly reduced the severity of pulmonary fibrosis and inflammatory cell accumulationin
107 n this study, an experimental mouse model of pulmonary fibrosis and lung samples from patients with I
108 o VEGF-Axxxb, are critical in development of pulmonary fibrosis and may be a paradigm for the regulat
109 as of lungs of both patients with idiopathic pulmonary fibrosis and mice that are subjected to a fibr
111 te that CHI3L1-dependent pathways exacerbate pulmonary fibrosis and suggest CHI3L1 as a potential bio
112 e progressively elevated in association with pulmonary fibrosis and that adenosine levels diminish in
113 ry epithelial proteinopathy with spontaneous pulmonary fibrosis and that autophagy is an important en
114 ociated with the progression of experimental pulmonary fibrosis and that this signaling pathway may m
115 nd when adenosine levels are elevated during pulmonary fibrosis and whether these elevations were ass
116 PP1, also known as osteopontin) increases in pulmonary fibrosis, and Spp1 transcription may be regula
117 collagen V overexpression during idiopathic pulmonary fibrosis, and these miRNAs may serve as pathog
118 se bone marrow failure, liver cirrhosis, and pulmonary fibrosis, and they increase susceptibility to
119 reidarsson syndrome, dyskeratosis congenita, pulmonary fibrosis, aplastic anemia, and liver fibrosis.
120 turnover predicts progression of idiopathic pulmonary fibrosis as determined by change in forced vit
121 ted in the lungs of patients with idiopathic pulmonary fibrosis as well as in wound healing and cance
122 n of VEGF-A165b inhibited the development of pulmonary fibrosis, as did treatment with intraperitonea
123 telomere-related diseases such as idiopathic pulmonary fibrosis, as well as in mice and other organis
124 ated genes previously implicated in familial pulmonary fibrosis-as significant contributors to sporad
125 to Confirm Efficacy and Safety in Idiopathic Pulmonary Fibrosis (ASCEND 016; 52 weeks)-for all-cause
127 or ingredient of SM, alleviates experimental pulmonary fibrosis both in vivo and in vitro by inhibiti
128 ative therapies in the treatment not only of pulmonary fibrosis, but also of a wide-ranging spectrum
129 rom bleomycin-treated donor mice exacerbated pulmonary fibrosis, but not if the donor cells were made
130 ed CD11c(+) cells promoted bleomycin-induced pulmonary fibrosis by activation of fibroblast telomeras
131 D treatment could prevent bleomycin-induced pulmonary fibrosis by delaying or suppressing ultrastruc
132 inflammation and, at 0.001 mg/kg, alleviates pulmonary fibrosis by increasing levels of the immunosup
133 sis including 262 unrelated individuals with pulmonary fibrosis clinically classified as IPF accordin
135 HI3L1 levels are higher in HPS patients with pulmonary fibrosis compared with those who remain fibros
136 ated to subsequent progression of idiopathic pulmonary fibrosis (defined as death or decline in force
137 ntrol participants, patients with idiopathic pulmonary fibrosis demonstrate excessive monocyte migrat
139 in India, followed by CTD-ILD and idiopathic pulmonary fibrosis; diagnoses varied between site invest
140 s congenita, aplastic anemia, and idiopathic pulmonary fibrosis disrupt the binding between the prote
143 istration (FDA)-approved drug for idiopathic pulmonary fibrosis, for its therapeutic effect in cGVHD
144 trolled trials of IFN-gamma-1b in idiopathic pulmonary fibrosis (GIPF-001 [NCT00047645] and GIPF-007
146 Furthermore, AEC2s from patients with severe pulmonary fibrosis have reduced cell surface HA and impa
147 telomerase genes TERT and TR cause familial pulmonary fibrosis; however, in telomerase-null mice, sh
148 channel, has been implicated in cardiac and pulmonary fibrosis; however, its role in asthma remains
149 evaluate the importance and role of AREG in pulmonary fibrosis, identify the cellular source of AREG
152 tages of bleomycin-induced injury attenuates pulmonary fibrosis in association, with reductions in AD
153 he results showed significant attenuation of pulmonary fibrosis in CKO relative to control mice, as e
154 pression and activity in the pathogenesis of pulmonary fibrosis in human IPF and in an experimental m
155 vival and resolved fibrosis in two models of pulmonary fibrosis in mice (intratracheal bleomycin and
158 a small molecule STAT-3 inhibitor, decreased pulmonary fibrosis in the intraperitoneal BLM model as a
159 r 10 days after bleomycin strongly attenuate pulmonary fibrosis in the mouse bleomycin model, and by
160 capacity of these probes to detect and stage pulmonary fibrosis in vivo was assessed in a mouse model
161 fibroblasts in vitro The role of miR-101 in pulmonary fibrosis in vivo was studied using adenovirus-
163 concept of precision medicine to idiopathic pulmonary fibrosis, in particular to search for genetic
165 C57BL/6 mice were used in a murine model of pulmonary fibrosis induced by an intratracheal instillat
166 thways leading, after lung tissue injury, to pulmonary fibrosis instead of normal healing, by mediati
168 ILD, including 456 patients with idiopathic pulmonary fibrosis (IPF) (men, 366; women, 90; median ag
169 e shared environmental exposures, idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmona
172 uted tomographic (CT) features of idiopathic pulmonary fibrosis (IPF) and to gain insight into the wa
173 hospitalizations of patients with idiopathic pulmonary fibrosis (IPF) are more frequent than those fo
174 y is related to poor outcome, and idiopathic pulmonary fibrosis (IPF) can be regarded as an exemplar.
175 g biopsy, patients diagnosed with idiopathic pulmonary fibrosis (IPF) in clinical practice could part
207 uals might be diagnosed as having idiopathic pulmonary fibrosis (IPF) or chronic (fibrotic) hypersens
209 (GER) is higher in patients with idiopathic pulmonary fibrosis (IPF) than in matched control subject
210 ce of a first-choice diagnosis of idiopathic pulmonary fibrosis (IPF) versus not IPF for MDTMs, clini
212 donors and patients with COPD or idiopathic pulmonary fibrosis (IPF), as well as in cigarette smoke-
213 ated approach to the diagnosis of idiopathic pulmonary fibrosis (IPF), based on a systematic search o
214 ity prediction is well studied in idiopathic pulmonary fibrosis (IPF), but little is known about pred
215 ients with stable and progressive idiopathic pulmonary fibrosis (IPF), defined as <5% and >/=10% decl
216 ive in slowing the progression of idiopathic pulmonary fibrosis (IPF), it remains a debilitating and
217 n lung tissues from patients with idiopathic pulmonary fibrosis (IPF), whereas PIAS4 protein levels a
218 sis-free) donors or patients with idiopathic pulmonary fibrosis (IPF), which is a very aggressive fib
230 implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF); however, the repertoire of aut
243 ular adenosine levels and the progression of pulmonary fibrosis is critical for designing adenosine b
245 rs to lung stem cell renewal and that severe pulmonary fibrosis is the result of distal epithelial st
246 elevance of precision medicine to idiopathic pulmonary fibrosis is yet to be established, but we beli
250 othelial and mesenchymal cells in idiopathic pulmonary fibrosis lungs but has limited or no expressio
251 Vs) are beneficial for acute lung injury and pulmonary fibrosis, mechanisms of mEV uptake by lung fib
252 own to be efficacious in a bleomycin-induced pulmonary fibrosis model in mice and in reducing extrace
255 In addition to the adverse effects caused by pulmonary fibrosis, most patients with IPF have associat
256 cell accumulationin in the bleomycin-induced pulmonary fibrosis mouse model on supplementary days 14,
258 y, and a provisional diagnosis of idiopathic pulmonary fibrosis or connective tissue disease-related
259 ed in peripheral blood cells from idiopathic pulmonary fibrosis patients and correlated with markers
265 ASM cells and fibroblasts from patients with pulmonary fibrosis (PF), chronic obstructive pulmonary d
266 Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with higher prevalence in older
268 Many patients with suspected idiopathic pulmonary fibrosis present with atypical high-resolution
270 Importantly, in a mouse model of idiopathic pulmonary fibrosis (RAGE-/-), reconstitution of RAGE eff
272 (0.0237), and treatment-emergent idiopathic-pulmonary-fibrosis-related (0.0132) mortality; similar r
273 t all-cause mortality (p=0.0420), idiopathic-pulmonary-fibrosis-related mortality (0.0237), and treat
274 0.72; 0.0029]; treatment-emergent idiopathic-pulmonary-fibrosis-related mortality 0.32 [0.14-0.76; 0.
275 rtality 0.45 [0.24-0.83; 0.0094]; idiopathic-pulmonary-fibrosis-related mortality 0.35 [0.17-0.72; 0.
276 mortality, and treatment-emergent idiopathic-pulmonary-fibrosis-related mortality at weeks 52, 72, an
277 ent-emergent all-cause mortality, idiopathic-pulmonary-fibrosis-related mortality, and treatment-emer
281 Studies Assessing Pirfenidone in Idiopathic Pulmonary Fibrosis: Research of Efficacy and Safety Outc
284 F lungs and from mice with bleomycin-induced pulmonary fibrosis showed an increased rate of prolifera
285 d using a bleomycin-instilled mouse model of pulmonary fibrosis showed that Salvianolic acid B (SAB),
286 s to Estimate Time-Progression in Idiopathic Pulmonary Fibrosis) study were used to conduct associati
287 igher in lungs from patients with idiopathic pulmonary fibrosis than in control individuals and were
289 In the murine model of bleomycin-induced pulmonary fibrosis, the consequences of matriptase deple
290 r epithelium is often associated with severe pulmonary fibrosis, the latter of which involves the rec
291 n of miR-877-3p as a fibrosis suppressor for pulmonary fibrosis therapy and also as a fibrosis marker
292 ibutes to the development and progression of pulmonary fibrosis through its regulation of ADORA2B exp
294 to Confirm Efficacy and Safety in Idiopathic Pulmonary Fibrosis] trial), including all patients rando
295 induced pulmonary fibrosis and in idiopathic pulmonary fibrosis, two diseases considered to be promot
296 ue stretch contributes to the development of pulmonary fibrosis via mechanotransduced activation of T
297 Over time, these mice develop spontaneous pulmonary fibrosis, which is ameliorated by restoration
298 tivity pneumonitis are at risk of developing pulmonary fibrosis, which is associated with reduced sur
299 ing cells led to increased bleomycin-induced pulmonary fibrosis, which is mediated by increased expre
300 s to develop a method to diagnose idiopathic pulmonary fibrosis without the patient having to undergo
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