ライフサイエンスコーパス: fibrotic response

1 d inflammation was followed by an attenuated fibrotic response.

2 ependent tissue injury eventually leads to a fibrotic response.

3 ac fibroblasts as principal mediators of the fibrotic response.

4 and SPARC mediate different aspects of this fibrotic response.

5 philia is not necessary for development of a fibrotic response.

6 e mice highlighted the reversibility of this fibrotic response.

7 block Ras/MEK/ERK signaling and abolish the fibrotic response.

8 these mice will have a significantly reduced fibrotic response.

9 rive myofibroblast formation and the cardiac fibrotic response.

10 key effector cells in the development of the fibrotic response.

11 New Zealand White rabbits failed to elicit a fibrotic response.

12 ollagen, suggesting a possible basis for the fibrotic response.

13 k between inflammatory potential and initial fibrotic response.

14 thogenic leukocyte subtypes, which drive the fibrotic response.

15 ory response was followed by a subsequent M2 fibrotic response.

16 her large, nor associated with a significant fibrotic response.

17 l heart regeneration, resulting in a default fibrotic response.

18 IPF lung fibroblasts reduced the exacerbated fibrotic response.

19 microvascular rarefaction with an exuberant fibrotic response.

20 astic alveolar epithelial cells regulate the fibrotic response.

21 and the emerging role of lymphocytes in the fibrotic response.

22 during chronic liver injury and mediate the fibrotic response.

23 ce of hematopoietically derived cells to the fibrotic response.

24 he expression of these mRNAs and enhance the fibrotic response.

25 events critical for the inflammatory and the fibrotic responses.

26 t at sites of Th2 inflammation and in tissue fibrotic responses.

27 s subpopulations that have distinct roles in fibrotic responses.

28 oxically elevated in murine lungs undergoing fibrotic responses.

29 modulate the heart's innate inflammatory and fibrotic responses.

30 ps of genes involved in the inflammatory and fibrotic responses.

31 ted partially to peritoneal inflammatory and fibrotic responses.

32 val, and increased lung inflammatory and pro-fibrotic responses.

33 f ROCK1 expectedly reduced TGF-beta1 induced fibrotic responses.

34 ontribution of LPA1/2/3 in mediating the pro-fibrotic responses.

35 mmation, wound healing, and their subsequent fibrotic responses.

36 causes prominent changes in hypertrophic and fibrotic responses accompanied by augmentation of Smad3/

37 of stimulating liver cell proliferation and fibrotic responses, accompanied by signs of oxidative st

38 The fibrotic response after diverse forms of injury is chara

39 hypothesized that it may play a role in the fibrotic response after injury.

40 pporting a role for MC bFGF in the pulmonary fibrotic response and its clinical consequence.

41 kinase within the fibroblast to program the fibrotic response and myofibroblast formation in vivo, s

42 ggest novel methods for the reduction of the fibrotic response and promotion of regeneration.

43 elastin and collagen expression, promoting a fibrotic response and subsequent stabilization of existi

44 ermore, poly(I:C) abrogated TGF-beta-induced fibrotic responses and blocked canonical Smad signaling

45 It is not clear how the hypertrophic and fibrotic responses are transcriptionally regulated.

46 clear anchorage in DKO mice coincided with a fibrotic response as indicated by increased collagen and

47 rkedly reduced the pressure overload-induced fibrotic response as well as fibrosis mediated by a hear

48 by impaired regeneration, inflammation, and fibrotic response at day 14, increased fat infiltration,

49 nesis of HP, amplifying the inflammatory and fibrotic response by paracrine signaling inducing the se

50 mportant structural cells can perpetuate the fibrotic response by regulating the differentiation, rec

51 ibroblasts, we investigated the induction of fibrotic responses by the S1P receptor (S1PR) agonists S

52 e persistence of necrotic cells stimulated a fibrotic response characterized by extensive collagen de

53 30-40 microm showed angiogenesis and reduced fibrotic response, coinciding with a shift in macrophage

54 otubule-localized TRPC3-GEF-H1 axis mediates fibrotic responses commonly in cardiac myocytes and fibr

55 nal deterioration followed by an exaggerated fibrotic response compared with control animals.

56 l mice, however, demonstrated enhanced early fibrotic responses compared with wild-type mice with pan

57 growth factor alone produce only a transient fibrotic response, connective tissue growth factor and t

58 The fibrotic response contained increased amounts of types I

59 ts position Egr-1 downstream of c-Abl in the fibrotic response, delineate a novel Egr-1-dependent int

60 n adipocytes is a critical component of the "fibrotic response," directly linked to metabolic dysfunc

61 l inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through down

62 nitric oxide participates in modulating the fibrotic response during the development of pulmonary gr

63 urrounded by a layer of CD3(+) T cells and a fibrotic response encapsulating the lesions were observe

64 mesenchymal transition (EMT) is important in fibrotic responses, formation of cancer stem cells, and

65 oint at a possible shift in inflammation and fibrotic response from adipose tissue to liver and a pos

66 to dietary induction of the inflammatory and fibrotic response genes.

67 Galectin-3 regulates inflammatory and fibrotic responses; however, its role in cardiac remodel

68 xpression was induced after the onset of the fibrotic response, IL-10, IL-13, and Stat6 dependent, an

69 e increased secretion of IL-1beta, induces a fibrotic response in adjacent airway fibroblasts.

70 is not only protective, but can reverse the fibrotic response in carbon tetrachloride-induced fibros

71 The fibrotic response in Clusterin deficient (CLU-/-) mice p

72 et failed to significantly contribute to the fibrotic response in either acute or chronic infection.

73 We investigated whether the enhanced fibrotic response in GM-CSF-/- animals was due to a defi

74 e hypothesis that MC bFGF contributes to the fibrotic response in human interstitial lung disease, we

75 (+) cells are sufficient to reconstitute the fibrotic response in IL-21R-deficient mice.

76 lates at least 50% of the renal interstitial fibrotic response in obstructive nephropathy, an effect

77 ch in turn may have a profound effect on the fibrotic response in SSc.

78 sed collagen expression, leading to an early fibrotic response in the abdominal aortic wall and resul

79 ngiotensin II infusion revealed a pronounced fibrotic response in the absence of miR145.

80 MRI allowed the visualization of the primary fibrotic response in the aortic wall.

81 underlying mesenchymal tissue demonstrated a fibrotic response in the dermis of the skin but not the

82 pulmonary inflammation and intensifying the fibrotic response in the patients.

83 ing dedifferentiation and contributes to the fibrotic response in the tubulointerstitium (TI) after u

84 The reduced fibrotic response in wounds from IL-1R KO mice could be

85 ZYZ-168 appeared to inhibit the fibrotic responses in a concentration dependent manner,

86 ponectin receptor agonists abrogated ex vivo fibrotic responses in explanted normal and SSc fibroblas

87 genesis after chronic colitis by stimulating fibrotic responses in fibroblasts.

88 In these rats, CRMS induces microvascular fibrotic responses in heart and kidneys, associated with

89 al TRPC3 inhibition significantly suppressed fibrotic responses in human cardiomyocytes and cardiac f

90 oth conjunctival inflammatory and subsequent fibrotic responses in patients with OCP.

91 od pressure control and for hypertrophic and fibrotic responses in the mouse heart and aorta.

92 elenting and destructive progression of most fibrotic responses in the pulmonary, cardiovascular, int

93 ay an important role in the inflammatory and fibrotic responses in viral and/or nonviral human airway

94 1 expression increases on fibroblasts during fibrotic responses in vivo, and IL-13 increases collagen

95 cin sulfate provoked lethal inflammatory and fibrotic responses in WT (CCR4(+/+)) mice, but such resp

96 ver of unrestrained wound healing (i.e., the fibrotic response) in these and other organ systems.

97 dence that implicate c-Abl as a mediator for fibrotic responses induced by transforming growth factor

98 ngs also imply that cellular homeostasis and fibrotic response involve the integration of signaling t

99 st lines into immunodeficient mice, and this fibrotic response is dependent on the interaction betwee

100 ess, but current evidence indicates that the fibrotic response is driven by abnormally activated alve

101 e I increased at 48 hours, suggesting that a fibrotic response is induced after the amniotic sac punc

102 genetically modified mice and show that the fibrotic response is largely independent of B and T lymp

103 One chemokine that is repeatedly linked to fibrotic responses is monocyte chemoattractant protein-1

104 13-PE inhibited silica-induced granuloma and fibrotic responses noted at 24 h and 15 d after the last

105 de (CGRP) in denervated kidneys mimicked the fibrotic response observed in innervated obstructed kidn

106 diated CD69 blockade in WT mice mimicked the fibrotic response of cd69(-/-) mice.

107 ts a functional role of this molecule in the fibrotic response of keratocytes to wound healing.

108 e alpha8beta1 integrin may contribute to the fibrotic response of organs to injury.

109 extracellular messenger, enhancing specific fibrotic responses of keratocytes to TGFbeta.

110 he liver by determining the inflammatory and fibrotic responses of nfkappab1-null mice in an experime

111 and in vivo loss of Sox9 blunted the cardiac fibrotic response on ischemic injury.

112 nd with either an augmented hypertrophic and fibrotic response or a diminished hypertrophy and resist

113 Inflammatory and fibrotic responses persisted for 4 mo in DBA/2J mice, wh

114 An unabated fibrotic response results in chronic liver disease and c

115 ssion profiles demonstrated inflammatory and fibrotic responses selectively in females.

116 These mice develop a robust fibrotic response similar to littermate genotype control

117 the S. rectivirgula-induced inflammatory and fibrotic response, suggesting that the CD4(+) T cell rep

118 ury incites an overwhelming inflammatory and fibrotic response that leads to expansive fibrous tissue

119 e the hyaluronan matrix without inducing pro-fibrotic responses that lead to nephropathy and proteinu

120 n and hepatocyte apoptosis, as well as early fibrotic responses; these findings indicate that shifts

121 as a global genomic regulator to direct the fibrotic response through its coordinated regulation of

122 lin/LRP1 co-complex in tissue remodeling and fibrotic responses through stimulation of anoikis resist

123 via A2B receptors to counterbalance the pro-fibrotic response to ATP.

124 ) mice showed a significantly increased lung fibrotic response to bleomycin compared with WT mice.

125 e to bleomycin, but reconstitutes their lung fibrotic response to bleomycin.

126 a-deficient mice that develop an exaggerated fibrotic response to determine whether changes in type 2

127 tic mediators in this model, we examined the fibrotic response to FITC in mice that were genetically

128 lammatory response to bleomycin, however the fibrotic response to injury was unaltered compared with

129 st that Th cytokine subsets can modulate the fibrotic response to injury.

130 regard to the capacity of MSCs to influence fibrotic response to liver injury and will explore the p

131 of stellate cells is a central event in the fibrotic response to liver injury, we hypothesized that

132 a macrophage membrane protein regulates the fibrotic response to lung injury and suggest a novel tar

133 of the maladaptive remodeling and myocardial fibrotic response to PO.

134 Estradiol replacement restored the fibrotic response to that of the intact female mice in t

135 cient (Sphk2(-/-)) mice showed an attenuated fibrotic response to UUO compared with wild-type mice, a

136 The lung fibrotic response to V(2)O(5) partially resolves where f

137 TLR4-, and C5aR-mediated proinflammatory and fibrotic responses to bacteria that were consistent with

138 P1(-/-) or EP3(-/-) mice, showed exaggerated fibrotic responses to bleomycin administration in vivo a

139 whether MMP-8 regulates lung inflammatory or fibrotic responses to bleomycin, we delivered bleomycin

140 ling and EndoMT in regulating angiogenic and fibrotic responses to injury.

141 that GRP blockade decreases inflammatory and fibrotic responses to radiation in mice.

142 temic disease processes, and inflammatory or fibrotic responses to stimuli.

143 , there was no evidence of resolution of the fibrotic response up to 45 days after bleomycin therapy.

144 ect effect on cardiac fibroblasts to inhibit fibrotic responses via extracellular signal-related kina

145 Fibrotic response was assessed by quantitative real time

146 e IL-13 receptor alpha-2-Fc, the exacerbated fibrotic response was completely inhibited.

147 ormally demonstrating that their exacerbated fibrotic response was due to heightened IL-13 activity.

148 established in both genotypes; however, the fibrotic response was profoundly worsened in Egr-1-defic

149 gammadelta T cells are effector cells in the fibrotic response, we performed adoptive transfer experi

150 otential role in modulating inflammatory and fibrotic responses, we examined the expression of the nu

151 nd its availability governs the intensity of fibrotic responses, we investigated p300 expression in S

152 eomycin or vehicle, and pulmonary injury and fibrotic responses were compared.

153 In this study, the lung fibrotic responses were investigated in COX-1 or COX-2-d

154 Fibrotic responses were studied using proliferation, mig

155 ng adiponectin mounted an exaggerated dermal fibrotic response, while transgenic mice with constituti

156 limited induction of PGE(2) and an enhanced fibrotic response with increased lung collagen content c