ライフサイエンスコーパス: fibrotic disease

1 ught to identify new therapeutic targets for fibrotic disease.

2 ntial therapeutic applications in cancer and fibrotic disease.

3 he pathologic microenvironment of cancer and fibrotic disease.

4 set destructive tissue remodeling in chronic fibrotic disease.

5 hibitors of the human P4H enzyme involved in fibrotic disease.

6 l of TGFbeta signaling and the prevention of fibrotic disease.

7 ibutes to severe inflammation and multiorgan fibrotic disease.

8 for therapy in this prototypic multisystemic fibrotic disease.

9 and, more importantly, at risk of pulmonary fibrotic disease.

10 er and stellate cell death in malignancy and fibrotic disease.

11 ant hepatitis in the absence of pre-existent fibrotic disease.

12 or KCP in attenuating the pathology of renal fibrotic disease.

13 syndecan 4 may alleviate scarring in chronic fibrotic disease.

14 to play important roles in wound healing and fibrotic disease.

15 onnective tissue growth factor might play in fibrotic disease.

16 of extracellular matrix protein synthesis in fibrotic disease.

17 ng development and in response to injury and fibrotic disease.

18 novel genetically determined animal model of fibrotic disease.

19 7 was administered during the progression of fibrotic disease.

20 in II blockade alone cannot stop progressive fibrotic disease.

21 be used to treat an established and ongoing fibrotic disease.

22 vels result in the relentless progression of fibrotic disease.

23 onary nodule 1-2 cm in diameter, and 20 with fibrotic disease.

24 ar matrix (ECM) clearance as a key factor in fibrotic disease.

25 pe that are predominant in wound healing and fibrotic disease.

26 for targeting the mesenchymal niche to treat fibrotic disease.

27 unknown trans- and cis-targets for treating fibrotic disease.

28 er preclinical development in the context of fibrotic disease.

29 vestigation into myeloid cells as drivers of fibrotic disease.

30 opathy, which correlates with progression of fibrotic disease.

31 erapeutic target for this difficult-to-treat fibrotic disease.

32 lating MC collagen expression, a hallmark of fibrotic disease.

33 a curative effect on scleroderma, a typical fibrotic disease.

34 1 may have translational effect for treating fibrotic disease.

35 tion is a key process in the pathogenesis of fibrotic disease.

36 flammatory cytokines and are dysregulated in fibrotic disease.

37 tissues might be used to treat patients with fibrotic diseases.

38 cal mechanisms involved in wound healing and fibrotic diseases.

39 rotein response (UPR) in the pathogenesis of fibrotic diseases.

40 the potential for application against other fibrotic diseases.

41 flexor tendons and other tissues as well as fibrotic diseases.

42 l therapeutic targets in inflammation-driven fibrotic diseases.

43 l therapeutic approach in treating pulmonary fibrotic diseases.

44 promising new therapeutic approach for human fibrotic diseases.

45 diovascular, neurological, inflammatory, and fibrotic diseases.

46 action may be useful in treating a number of fibrotic diseases.

47 on by fibroblasts contributes to scarring in fibrotic diseases.

48 of modifying the deleterious effects of the fibrotic diseases.

49 gnature" that can be used as a biomarker for fibrotic diseases.

50 ent pose an enormous challenge when treating fibrotic diseases.

51 lopment of targeted therapies for individual fibrotic diseases.

52 ch with broad applicability in oncologic and fibrotic diseases.

53 ew role for tumor suppressors in attenuating fibrotic diseases.

54 gy for controlling myofibroblasts in chronic fibrotic diseases.

55 ypertrophic scarring and in the treatment of fibrotic diseases.

56 vide therapeutic opportunities to treat oral fibrotic diseases.

57 athophysiological relevance across different fibrotic diseases.

58 l treatment for systemic sclerosis and other fibrotic diseases.

59 the potential to treat mast cell associated fibrotic diseases.

60 therapeutic strategies for the treatment of fibrotic diseases.

61 ynamic, unrelenting process propelling human fibrotic diseases.

62 for intimal hyperplasia, wound healing, and fibrotic diseases.

63 may prove effective for a variety of chronic fibrotic diseases.

64 erentiation of myofibroblasts, a hallmark of fibrotic diseases.

65 diseases including cancer and autoimmune and fibrotic diseases.

66 argeting hyperactive Smad signaling in renal fibrotic diseases.

67 therapies for both inflammatory and chronic fibrotic diseases.

68 o prevent and treat several inflammatory and fibrotic diseases.

69 rvention and prevention of keloids and other fibrotic diseases.

70 uction in patients with scleroderma or other fibrotic diseases.

71 -beta1) is thought to play a crucial role in fibrotic diseases.

72 hway could provide a novel treatment in many fibrotic diseases.

73 sts is an effective therapeutic strategy for fibrotic diseases.

74 ase collagen overproduction in SSc and other fibrotic diseases.

75 rapeutic approach in inflammatory as well as fibrotic diseases.

76 drive disease progression in later stages of fibrotic diseases.

77 in the treatment of chronic inflammatory and fibrotic diseases.

78 el therapeutic strategy for the treatment of fibrotic diseases.

79 to the control of hepatic granulomatous and fibrotic diseases.

80 ctive therapies for patients with recognized fibrotic diseases.

81 ently no effective therapies for progressive fibrotic diseases.

82 ive collagen imaging across a range of human fibrotic diseases.

83 screening assays of candidate treatments for fibrotic diseases.

84 tential therapeutic resolution of persistent fibrotic diseases.

85 ell-documented roles in tumor metastasis and fibrotic diseases.

86 anisms that parallel those observed in other fibrotic diseases.

87 ynthesis of type I collagen is a hallmark of fibrotic diseases.

88 cell communication in the pathophysiology of fibrotic diseases.

89 tic cancer as well as in patients with other fibrotic diseases.

90 eptor implicated in several inflammatory and fibrotic diseases.

91 icated in the development and progression of fibrotic diseases.

92 ic agent and its application in experimental fibrotic diseases.

93 ntagonists could be effective agents against fibrotic diseases.

94 rug candidates for treating inflammatory and fibrotic diseases.

95 y, collagen and elastin, and is indicated in fibrotic diseases.

96 has been linked to cancer, inflammatory, and fibrotic diseases.

97 roptosis may be beneficial in treating these fibrotic diseases.

98 sm is a therapeutic target for IPF and other fibrotic diseases.

99 ting avenues for more effective therapies in fibrotic diseases.

100 th potentially broader applications in other fibrotic diseases.

101 balance checkpoint and therapeutic target in fibrotic diseases.

102 preclinical development for the treatment of fibrotic diseases.

103 s deemed relevant for cardiopulmonary and/or fibrotic diseases.

104 rtunities for the treatment of SSc and other fibrotic diseases.

105 levels leads to metabolic, inflammatory, and fibrotic diseases.

106 for efficacy studies in cirrhosis and other fibrotic diseases.

107 and mitochondrial dysfunction is involved in fibrotic diseases.

108 is a promising approach for the treatment of fibrotic diseases.

109 otential roles of molecular imaging in human fibrotic diseases.

110 development of therapeutic interventions in fibrotic diseases.

111 cates potential therapeutic targets for lung fibrotic diseases.

112 tory conditions, while TGF-B is increased in fibrotic diseases.

113 ed receptor associated with inflammatory and fibrotic diseases.

114 arterial and venous thrombosis, and chronic fibrotic diseases.

115 cessive deposition of type I collagen causes fibrotic diseases.

116 tial therapeutic targets in the treatment of fibrotic diseases.

117 present a novel opportunity to target deadly fibrotic diseases.

118 is a potential therapeutic strategy to treat fibrotic diseases.

119 neficial effects to block the progression of fibrotic diseases.

120 g from cardiovascular and renal disorders to fibrotic diseases.

121 red as a potential therapy for patients with fibrotic diseases.

122 f UCHL1 as a potential therapeutic target in fibrotic diseases.

123 ellular homeostasis in aging and age-related fibrotic diseases.

124 reatment of human cardiac fibrosis and other fibrotic diseases.

125 esponse in aging contributing to age-related fibrotic diseases.

126 has potential as a therapeutic approach for fibrotic diseases.

127 e and aid in the prevention and treatment of fibrotic diseases.

128 ng IL-25 and ILC2 for the treatment of human fibrotic diseases.

129 n cancers, atherosclerosis, and a variety of fibrotic diseases.

130 as a novel potential therapeutic target for fibrotic diseases.

131 healing and its persistence is a hallmark of fibrotic diseases.

132 treatment of patients with a broad range of fibrotic diseases.

133 histamine plays an important role in painful fibrotic diseases.

134 Fibrotic diseases affect multiple organs and are associa

135 Systemic sclerosis (SSc) is a spreading fibrotic disease affecting the skin and internal organs.

136 e highlight therapeutic strategies to rescue fibrotic disease after the resolution of acute disease,

137 fferences, it was assumed that the different fibrotic diseases also have different pathomechanisms.

138 ticulum (ER) stress is an emerging factor in fibrotic disease, although precise mechanisms are not cl

139 endocytosis, is a potential target to treat fibrotic diseases, although the mechanisms and responsib

140 mporomandibular joint disorders, caries, and fibrotic diseases among different organs, as well as to

141 nical implications for both the treatment of fibrotic disease and cancer.

142 development and wound healing, and occurs in fibrotic disease and carcinoma.

143 a is also the central pathogenic cytokine in fibrotic disease and likely promotes pneumonitis.

144 nse, and is implicated in the progression of fibrotic diseases and cancer.

145 levels as potential therapeutic targets for fibrotic diseases and cancer.

146 fate of myofibroblasts in various important fibrotic diseases and describe how manipulation of macro

147 iven that TGF-beta has been shown to promote fibrotic diseases and desmoplasia, identifying the fibro

148 omplex biological mechanisms responsible for fibrotic diseases and developing effective therapies.

149 Despite the growing incidence of fibrotic diseases and extensive research efforts, there

150 TN-C is re-expressed during wound healing, fibrotic diseases and in cancer.

151 d healing, is overexpressed in a majority of fibrotic diseases and in various tumors.

152 expression in the skin was elevated in all 3 fibrotic diseases and is a driver of tenascin C (TNC) pr

153 ant autophagy and deregulated epigenetics in fibrotic diseases and may contribute to the development

154 tive and novel approach for the treatment of fibrotic diseases and modulation of profibrogenic effect

155 ed in the hyper-activation of fibroblasts in fibrotic diseases and the activation of pancreatic stell

156 rovide new insights into the pathogenesis of fibrotic diseases and the development of drugs for their

157 The prevalence of fibrotic diseases and the lack of pharmacologic modaliti

158 pproaches for improving clinical outcomes in fibrotic diseases and wound healing.

159 en the link between TGF-beta1 expression and fibrotic disease, and demonstrate the potency of TGF-bet

160 icated in several diseases including cancer, fibrotic diseases, and inflammation, among others.

161 phospholipid signaling, bone mineralization, fibrotic diseases, and tumor-associated immune cell infi

162 chanisms underlying cancer-recruited stroma, fibrotic diseases, and wound-healing responses.

163 Fibrotic diseases are a significant global burden for wh

164 Fibrotic diseases are characterized by progressive and o

165 Fibrotic diseases are involved in 45% of deaths in the U

166 Fibrotic diseases are not well-understood.

167 As fibrotic diseases are often molecularly heterogeneous, m

168 The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibro

169 Because fibrotic diseases are typically progressive disorders, a

170 d tissue remodeling in IPF and perhaps other fibrotic diseases as well.

171 Interleukin 13 (IL-13) is a key factor in fibrotic disease associated with helminth infection, but

172 being developed for schistosomiasis or other fibrotic diseases associated with a T-helper 2 cell-medi

173 identified as a target for the treatment of fibrotic diseases, based on the role it has in activatin

174 critical driver of collagen accumulation and fibrotic disease but also a vital suppressor of inflamma

175 s a potential therapy for cardiovascular and fibrotic diseases, but its short in vivo half-life is an

176 critical event in the pathogenesis of human fibrotic diseases, but regulatory mechanisms for this ef

177 drome, lung adenocarcinoma, and debilitating fibrotic diseases, but the critical transcription factor

178 aling through one of its receptors, LPA1, in fibrotic diseases, but the mechanisms by which LPA-LPA1

179 lungs and contribute to remodelling in other fibrotic diseases, but their involvement in allergic ast

180 TGFB induces autophagy in fibrotic diseases by SMAD3-dependent downregulation of t

181 ic target for a number of diseases including fibrotic diseases, cancer, and inflammation, among other

182 thway will be highly effective at preventing fibrotic disease caused by chronic Th2-mediated inflamma

183 ial of gene therapy as a novel treatment for fibrotic diseases caused by TGF-beta1.

184 iopathic pulmonary fibrosis is a progressive fibrotic disease characterized by excessive deposition o

185 subglottic stenosis (iSGS) is a progressive fibrotic disease characterized by life-threatening airwa

186 ay be important in the pathogenesis of human fibrotic diseases characterized by overexpression/activa

187 and more effective therapeutic strategy for fibrotic diseases characterized by persistent myofibrobl

188 SMAD7 has been reported in TGF-beta-mediated fibrotic diseases, characterized by overproduction of co

189 rogression, tumorigenesis, neuropathic pain, fibrotic diseases, cholestatic pruritus, lymphocyte homi

190 Fibrotic diseases display mesenchymal cell (MC) activati

191 GF-beta1, a central pathological mediator of fibrotic diseases, enhanced miR-21 expression in primary

192 In fibrotic diseases, fibroblasts synthesize abundant amoun

193 c approach to treating scleroderma and other fibrotic diseases finds support in animal studies and an

194 SignificanceTissue fibrotic diseases, for example of the liver and lung, re

195 Studies of patients with fibrotic diseases have demonstrated changes in component

196 Preclinical models of fibrotic diseases have implicated IL-13 activity on mult

197 in increased numbers in a variety of chronic fibrotic diseases; however, their role in the developmen

198 olved in the pathogenesis of a proto-typical fibrotic disease, idiopathic pulmonary fibrosis (IPF).

199 in the design of therapeutic modalities for fibrotic disease in the cornea and other parts of the ey

200 and MSC-like cells in myofibroblast-mediated fibrotic disease in the kidney, lung, heart, liver, skin

201 cific gene signature may assist in targeting fibrotic diseases in a more precise, organ-specific mann

202 D in three different in vivo mouse models of fibrotic diseases in a therapeutic setting.

203 exploration of CLDN1-targeting therapies for fibrotic diseases in patients.

204 enchymal transition (EMT) is associated with fibrotic diseases in the lens, such as anterior subcapsu

205 broblast differentiation in inflammatory and fibrotic diseases in the skin.

206 lasminogen activation system on TGF-beta1 in fibrotic diseases in vivo, as well as novel prognostic a

207 n signaling, a pathway implicated in several fibrotic diseases, in RPE cells in proliferative vitreor

208 TGFbeta has been implicated in promoting fibrotic diseases including CR, but is beneficial in the

209 may be a therapeutic target for treatment of fibrotic diseases including IPF.

210 licated in aberrant fibroblast activation in fibrotic diseases including systemic sclerosis (SSc).

211 o be involved in the pathobiology of various fibrotic diseases, including glaucoma.

212 TGF-beta has an established role in many fibrotic diseases, including glomerulosclerosis, where i

213 n of ECM components are dominant features of fibrotic diseases, including hepatic fibrosis.

214 Pathogenic fibrotic diseases, including idiopathic pulmonary fibros

215 investigated clinically for the treatment of fibrotic diseases, including idiopathic pulmonary fibros

216 investigated clinically for the treatment of fibrotic diseases, including idiopathic pulmonary fibros

217 Here, we demonstrate that many endstage fibrotic diseases, including IPF; scleroderma; myelofibr

218 role in the pathogenesis of inflammatory and fibrotic diseases, including radiation-induced fibrosis.

219 extracellular matrix is the hallmark of many fibrotic diseases, including systemic sclerosis and pulm

220 bute to the chronic organelle stress in many fibrotic diseases, including those of the lung and liver

221 g angiogenesis, autoimmune diseases, cancer, fibrotic diseases, inflammation, neurodegeneration, and

222 phages and fibroblasts play central roles in fibrotic disease initiation, maintenance, and progressio

223 lerosis (SSc) is a prototypical inflammatory fibrotic disease involving inflammation, vascular abnorm

224 Progressive fibrotic diseases involving diverse organ systems are as

225 o apoptosis are cardinal features of chronic fibrotic diseases involving diverse organ systems.

226 Fibrotic disease is associated with matrix deposition th

227 Fibrotic disease is caused by the continuous deposition

228 A hallmark of fibrotic disease is the excessive accumulation of extrac

229 eutic intervention in human inflammatory and fibrotic diseases is also discussed.

230 One paradigm that pervades all fibrotic diseases is the pathological myofibroblast, a c

231 plasminogen activator inhibitor-1 (PAI-1) in fibrotic diseases is well documented, its role in cardia

232 (CTGF/CCN2), associated with multiple human fibrotic diseases, is overexpressed in the tissue of gin

233 To understand the molecular basis of fibrotic disease, it is essential to appreciate how matr

234 IL-13) in systemic sclerosis (SSc) and other fibrotic diseases, its mechanisms of action are not unde

235 urthermore, these mechanisms are involved in fibrotic disease itself, with some miRs and epigenetic d

236 rocess of fibrosis, a deadly complication of fibrotic diseases like scleroderma (SSc).

237 gments in the plasma of patients with severe fibrotic disease may be a product of CTGF proteolysis th

238 the persistent activity of myofibroblasts in fibrotic diseases might involve epigenetic modifications

239 e harness the pathophysiological features of fibrotic diseases, namely leaky vasculature and aberrant

240 llowing lens injury and were responsible for fibrotic disease of the lens that occurs following catar

241 ulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology.

242 creatitis (CP) is a chronic inflammatory and fibrotic disease of the pancreas with a prevalence of 42

243 Idiopathic pulmonary fibrosis (IPF) is a fibrotic disease of unknown etiology that results in sig

244 candidate for the treatment of chronic renal fibrotic diseases of diverse etiologies is warranted.

245 nly for chronic kidney disease, but also for fibrotic diseases of other organs.

246 tractional force is a contributing factor to fibrotic diseases of the eye, such as proliferative vitr

247 diseases including arterial restenosis, and fibrotic diseases of the lung, liver, and kidney.

248 at the various stages in the development of fibrotic diseases of the lungs and other organs.

249 umonias (IIPs) are a collection of pulmonary fibrotic diseases of unknown etiopathogenesis.

250 ple organs, providing exciting insights into fibrotic disease pathogenesis.

251 The cause of fibrotic diseases, pathologies characterized by excessiv

252 t protein-1 chemokine receptor, CCR2, to the fibrotic disease process.

253 t provided a measure of the extent of active fibrotic disease progression and correlated strongly wit

254 en FSR correlates with established risks for fibrotic disease progression in NASH, and plasma lumican

255 o monitor the contribution of macrophages to fibrotic disease progression in the bleomycin-induced mu

256 re studies using FAPI PET/CT as a measure of fibrotic disease progression risk or response to antiinf

257 ggesting a buffering effect of hyaluronan on fibrotic disease progression.

258 Fibrotic diseases remain a major cause of morbidity and

259 d, their interplay in the context of chronic fibrotic diseases remains incompletely understood.

260 n of PU.1 expression is perturbed in various fibrotic diseases, resulting in the upregulation of PU.1

261 TGF in fibroblasts, and in patients with the fibrotic disease scleroderma.

262 ensing process in complex tissues, including fibrotic disease states with high collagen, is now utili

263 phogenesis, and that becomes dysregulated in fibrotic disease states.

264 potential therapeutic target for progressive fibrotic disease such as idiopathic pulmonary fibrosis (

265 is a promising approach to the treatment of fibrotic disease such as idiopathic pulmonary fibrosis.

266 nective tissue growth factor is expressed in fibrotic disease such as scleroderma, where it is believ

267 is a prominent feature of chronic pulmonary fibrotic diseases such as idiopathic interstitial pneumo

268 ta promotes excessive collagen deposition in fibrotic diseases such as idiopathic pulmonary fibrosis

269 plicated in the deposition of ECM protein in fibrotic diseases such as pulmonary fibrosis and atheros

270 Fibrotic diseases such as scleroderma, severe chronic as

271 CTGF to be a rational target for therapy in fibrotic diseases such as SSc.

272 a, which might be relevant to the genesis of fibrotic diseases such as SSc.

273 two cell types are a hallmark of progressive fibrotic diseases such as systemic sclerosis (also known

274 wounds, in the stroma of some tumors, and in fibrotic diseases such as systemic sclerosis (SSc) and r

275 ivo functional studies of candidate genes in fibrotic diseases such as systemic sclerosis.

276 destructive tissue remodeling that occurs in fibrotic diseases such as TED.

277 in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary fibrosis

278 in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary fibrosis

279 erapeutics in treating clinically refractory fibrotic diseases, such as IPF.

280 urrent bleak outlook for chronic progressive fibrotic diseases, such as scleroderma, due to lack of e

281 hibitory effects of sST2 in inflammatory and fibrotic diseases, suggesting that IL-33/ST2 is a unique

282 Systemic sclerosis is a fibrotic disease that initiates in the skin and progress

283 which distinguishes the condition from most fibrotic diseases that are progressive and irreversible.

284 r CKD and potentially other inflammatory and fibrotic diseases that avoids the adverse events associa

285 This concept is exemplified by fibrotic diseases that develop as a consequence of tissu

286 ta has emerged as central effector of MD and fibrotic disease, the cell types in diseased muscle that

287 Leukemic, polycythemic, or fibrotic disease transformation in essential thrombocyth

288 In the past few decades, its role in fibrotic diseases triggered the search for orally availa

289 This approach holds promise in fibrotic diseases unsuited for protein injection.

290 Generation of models for fibrotic disease using pluripotent stem cells is importa

291 ugh it has not been previously implicated in fibrotic disease, we found that Dril1 was highly express

292 ixed connective tissue disease, two systemic fibrotic diseases, were less able to inhibit fibrocyte d

293 ne the role of PI3K activation in human lung fibrotic disease, which could be amenable to targeted th

294 ggest that EpiC-FBs have utility in modeling fibrotic diseases while SHF-FBs are a promising source o

295 pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis.

296 Systemic sclerosis (SSc) is a multi-organ fibrotic disease with few treatment options.

297 clerosis (scleroderma, SSc) is a devastating fibrotic disease with few treatment options.

298 rogressive and irreversible inflammatory and fibrotic disease with no cure.

299 clerosis (SSc) is a clinically heterogeneous fibrotic disease with no effective treatment.

300 kine CXCL4 is implicated in inflammatory and fibrotic diseases, with CXCL4 proposed to potentiate TLR