戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 the Hsp90alpha isoform in the development of skin fibrosis.
2 mechanisms that lead to NUDT21 repression in skin fibrosis.
3 pe 2 alarmin cytokines in the mouse model of skin fibrosis.
4 with SSc and required for the maintenance of skin fibrosis.
5 tient age, and correlates with the extent of skin fibrosis.
6 ify common and specific features of lung and skin fibrosis.
7 fficacy in rodent models of lung, liver, and skin fibrosis.
8 ell death, in 2 murine models of scleroderma skin fibrosis.
9 romote collagen accumulation and features of skin fibrosis.
10 hat fresolimumab rapidly reverses markers of skin fibrosis.
11 atosclerosis, a condition of excessive human skin fibrosis.
12 stroesophageal reflux, renal impairment, and skin fibrosis.
13 m SSc patients correlates with the extent of skin fibrosis.
14 17 signaling has been implicated in lung and skin fibrosis.
15 a significant reduction in fibrocytes and in skin fibrosis.
16 ibrocytes in the generation of IL-13-induced skin fibrosis.
17 s adenosine and adenosine A(2A) receptors to skin fibrosis.
18 that SFRP4 may modulate Wnt functions in Tsk skin fibrosis.
19  human disorder characterized by progressive skin fibrosis.
20 umulation of collagen and the development of skin fibrosis.
21 ) is an auto-immune disease characterized by skin fibrosis.
22 e oral mucosa and sufficient to limit facial skin fibrosis.
23 venue for the treatment of lipodystrophy and skin fibrosis.
24 at exhibits promising potential for treating skin fibrosis.
25 ulations in SSc may drive the progression of skin fibrosis.
26 Sc into those with progressive versus stable skin fibrosis.
27 kewise, we found IL-33 upregulation in human skin fibrosis.
28 2) as a new profibrotic mediator in lung and skin fibrosis.
29 is a subset of SSc defined by the absence of skin fibrosis.
30  keratinocyte-derived signals as triggers of skin fibrosis.
31  subcutaneous bleomycin injections developed skin fibrosis accompanied by elevated IL-33 expression i
32 e signaling to regulatory T cells suppresses skin fibrosis and highlight a potential therapeutic axis
33 SCs, which was associated with reductions in skin fibrosis and improved skin function.
34 d fibronectin, and (3) attenuated late-stage skin fibrosis and inflammation induced by bleomycin.
35 lerosis is a complex disease with widespread skin fibrosis and variable visceral organ involvement.
36 ) spontaneously developed severe dermatitis, skin fibrosis, and systemic T helper type 2 immunity, su
37 onstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 i
38     Skin wound healing and bleomycin-induced skin fibrosis are thought to reflect complex interaction
39 l standards for patient assessment is to use skin fibrosis as an indicator of organ involvement, thou
40 nt yet not fully understood role of STAT6 in skin fibrosis by driving innate inflammation and differe
41 4 and - 13 contribute to the pathogenesis of skin fibrosis by promoting collagen production and myofi
42 bited tumor growth, and mitigated RT-induced skin fibrosis by targeting senescent fibroblasts, withou
43                           When dysregulated, skin fibrosis can lead to a multitude of pathologies.
44             Fibroblast STAT1 is required for skin fibrosis development in mice.
45 s, adipocyte lipolysis occurred early during skin fibrosis development, and lipid storage was re-esta
46 e survival and skin manifestations (onset of skin fibrosis, digital ulcers, telangiectasias, puffy fi
47        Scleroderma patients with progressive skin fibrosis display an IFN-regulated gene signature, i
48                                       During skin fibrosis, extracellular matrix proteins are overpro
49 sion and mitigates chronic radiation-induced skin fibrosis, highlighting a potential role for DFO in
50             Proteomic comparison of lung and skin fibrosis identified a common upregulation of margin
51 ate aberrant adiponectin pathway activity in skin fibrosis, identifying a novel function for this ple
52 ents, and the effects of anti-TGF-beta Ab on skin fibrosis, immune cell activation markers, and colla
53 r (ST2 knockout) showed markedly exacerbated skin fibrosis in association with significantly increase
54 ificantly reduced existing lung fibrosis and skin fibrosis in experimental models.
55 r its pharmacological inhibition, ameliorate skin fibrosis in experimental mouse models.
56  These data indicate that the progression of skin fibrosis in IL-13-induced AD occurs via TSLP/TSLPR-
57  miR-181b were elevated in bleomycin-induced skin fibrosis in mice and primary fibroblasts isolated f
58 181b inhibitors attenuated bleomycin-induced skin fibrosis in mice in association with decreased NUDT
59 Importantly, DMF prevented bleomycin-induced skin fibrosis in mice.
60 s required for loss of adipose tissue during skin fibrosis in mice.
61           The molecular mechanisms governing skin fibrosis in murine sclerodermatous graft-versus-hos
62 ymorphisms (SNPs) and predict the degrees of skin fibrosis in patients.
63 ggesting that the Wnt pathway might regulate skin fibrosis in SSc.
64 TAT6 plays a role during the pathogenesis of skin fibrosis in SSc.
65 The only independent factor for the onset of skin fibrosis in ssSSc was the positivity for anti-Scl-7
66 have suggested that Wnts might contribute to skin fibrosis in systemic sclerosis (SSc) by affecting t
67                                              Skin fibrosis in systemic sclerosis (SSc) is accompanied
68 novel model for studying the pathogenesis of skin fibrosis in systemic sclerosis.
69 rs a novel, non-invasive method of assessing skin fibrosis in the multisystem disease systemic sclero
70 issue disorders such as Marfan's syndrome or skin fibrosis in the tight skin mouse model of scleroder
71                                              Skin fibrosis in the TSK mouse, a model of skin fibrosis
72   It also suggests that MAGP-2 might mediate skin fibrosis in TSK mice and in patients with scleroder
73 ),ST2(flox/flox)) showed significantly worse skin fibrosis, increased T helper 2 to regulatory T cell
74                                 Furthermore, skin fibrosis induced by bleomycin administration is als
75 l disruption of TLR4 signaling in vitro, and skin fibrosis induced by bleomycin in vivo was attenuate
76                                     Moreover skin fibrosis induced by bleomycin was dependent on endo
77 1 as a key determinant in the development of skin fibrosis induced by bleomycin, and suggest that MCP
78 mad3-null (Smad3(-/-)) mice using a model of skin fibrosis induced by subcutaneous injections of bleo
79 ight-skin (Tsk) mouse, an animal model where skin fibrosis is caused by an in-frame duplication in fi
80 overy provides insight into the mechanism of skin fibrosis manifested by Tsk2/+ mice.
81                           The development of skin fibrosis may lead to patient discomfort, limitation
82 vo therapeutic efficacy in bleomycin-induced skin fibrosis model in mice.
83   These findings were also confirmed using a skin fibrosis model in which multiple injections of fibr
84 velopment of fibrosis in a bleomycin induced skin fibrosis mouse model.
85 p visit; ssSSc was defined by the absence of skin fibrosis (mRSS = 0 and no sclerodactyly) at all ava
86 emonstrated to induce impressive reversal of skin fibrosis, neoangiogenesis, improved functionality a
87              In a model of bleomycin-induced skin fibrosis, Nfkb1(-/-) and c-Rel(-/-) mice displayed
88 th STAT6 inhibitor AS1517499 also attenuated skin fibrosis on day 28.
89 findings provide insight into the effects of skin fibrosis on DWAT ADSCs, identify a DC-ADSC survival
90 wever, the main cellular participants in SSc skin fibrosis remain incompletely understood.
91   Skin fibrosis in the TSK mouse, a model of skin fibrosis seen in systemic sclerosis (SSc), is cause
92 rmal remodeling and is associated with human skin fibrosis severity.
93 tion of Hsp90alpha in experimental models of skin fibrosis such as human fibroblasts, C57BL/6 mice, a
94 tions in fibrillin-1 recapitulate aggressive skin fibrosis that is prevented by integrin-modulating t
95 ht skin (Tsk) mouse is an important model of skin fibrosis that occurs in systemic sclerosis.
96  a rare autoimmune disorder characterised by skin fibrosis that often also affects internal organs, e
97         In vivo, TLY012 reverses established skin fibrosis to near-normal skin architecture in mouse
98                     Despite the frequency of skin fibrosis, treatments that seek to address the root
99                             A feature of the skin fibrosis typical of scleroderma is atrophy of the d
100 ies have suggested that fibrillin 1 mediates skin fibrosis via its interface with associated microfib
101                   Red light (RL) may improve skin fibrosis via photobiomodulation, the process by whi
102 SSc-relevant pathways and alleviation of the skin fibrosis was remarkable in the inflammatory subsets
103 foothold in the pathogenesis of pathological skin fibrosis, we studied stiff skin syndrome (SSS), a r
104 clinical and histopathological parameters of skin fibrosis, whereas signatures of CXCL12+ and PI16+ f
105 dermal adipocyte lipodystrophy occurs during skin fibrosis, which compromises the skin's flexibility
106 /-) mice were resistant to bleomycin-induced skin fibrosis, which suggests a key role for the inflamm
107 sorder leading to childhood onset of diffuse skin fibrosis with autosomal dominant inheritance and co
108 ably, mice lacking Spag17 showed spontaneous skin fibrosis with increased dermal thickness, collagen

 
Page Top