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1 set destructive tissue remodeling in chronic fibrotic disease.
2 hibitors of the human P4H enzyme involved in fibrotic disease.
3 l of TGFbeta signaling and the prevention of fibrotic disease.
4 ibutes to severe inflammation and multiorgan fibrotic disease.
5 for therapy in this prototypic multisystemic fibrotic disease.
6 and, more importantly, at risk of pulmonary fibrotic disease.
7 er and stellate cell death in malignancy and fibrotic disease.
8 ant hepatitis in the absence of pre-existent fibrotic disease.
9 or KCP in attenuating the pathology of renal fibrotic disease.
10 syndecan 4 may alleviate scarring in chronic fibrotic disease.
11 to play important roles in wound healing and fibrotic disease.
12 onnective tissue growth factor might play in fibrotic disease.
13 of extracellular matrix protein synthesis in fibrotic disease.
14 ng development and in response to injury and fibrotic disease.
15 novel genetically determined animal model of fibrotic disease.
16 7 was administered during the progression of fibrotic disease.
17 in II blockade alone cannot stop progressive fibrotic disease.
18 be used to treat an established and ongoing fibrotic disease.
19 onary nodule 1-2 cm in diameter, and 20 with fibrotic disease.
20 opathy, which correlates with progression of fibrotic disease.
21 erapeutic target for this difficult-to-treat fibrotic disease.
22 lating MC collagen expression, a hallmark of fibrotic disease.
23 a curative effect on scleroderma, a typical fibrotic disease.
24 1 may have translational effect for treating fibrotic disease.
25 tion is a key process in the pathogenesis of fibrotic disease.
26 flammatory cytokines and are dysregulated in fibrotic disease.
27 ntial therapeutic applications in cancer and fibrotic disease.
28 he pathologic microenvironment of cancer and fibrotic disease.
29 ew role for tumor suppressors in attenuating fibrotic diseases.
30 gy for controlling myofibroblasts in chronic fibrotic diseases.
31 ypertrophic scarring and in the treatment of fibrotic diseases.
32 vide therapeutic opportunities to treat oral fibrotic diseases.
33 l treatment for systemic sclerosis and other fibrotic diseases.
34 the potential to treat mast cell associated fibrotic diseases.
35 therapeutic strategies for the treatment of fibrotic diseases.
36 ynamic, unrelenting process propelling human fibrotic diseases.
37 may prove effective for a variety of chronic fibrotic diseases.
38 erentiation of myofibroblasts, a hallmark of fibrotic diseases.
39 diseases including cancer and autoimmune and fibrotic diseases.
40 argeting hyperactive Smad signaling in renal fibrotic diseases.
41 therapies for both inflammatory and chronic fibrotic diseases.
42 rvention and prevention of keloids and other fibrotic diseases.
43 uction in patients with scleroderma or other fibrotic diseases.
44 -beta1) is thought to play a crucial role in fibrotic diseases.
45 hway could provide a novel treatment in many fibrotic diseases.
46 sts is an effective therapeutic strategy for fibrotic diseases.
47 ase collagen overproduction in SSc and other fibrotic diseases.
48 in the treatment of chronic inflammatory and fibrotic diseases.
49 el therapeutic strategy for the treatment of fibrotic diseases.
50 to the control of hepatic granulomatous and fibrotic diseases.
51 ently no effective therapies for progressive fibrotic diseases.
52 present a novel opportunity to target deadly fibrotic diseases.
53 is a potential therapeutic strategy to treat fibrotic diseases.
54 neficial effects to block the progression of fibrotic diseases.
55 g from cardiovascular and renal disorders to fibrotic diseases.
56 red as a potential therapy for patients with fibrotic diseases.
57 ellular homeostasis in aging and age-related fibrotic diseases.
58 reatment of human cardiac fibrosis and other fibrotic diseases.
59 esponse in aging contributing to age-related fibrotic diseases.
60 cessive deposition of type I collagen causes fibrotic diseases.
61 has potential as a therapeutic approach for fibrotic diseases.
62 e and aid in the prevention and treatment of fibrotic diseases.
63 ng IL-25 and ILC2 for the treatment of human fibrotic diseases.
64 n cancers, atherosclerosis, and a variety of fibrotic diseases.
65 as a novel potential therapeutic target for fibrotic diseases.
66 healing and its persistence is a hallmark of fibrotic diseases.
67 treatment of patients with a broad range of fibrotic diseases.
68 histamine plays an important role in painful fibrotic diseases.
69 tial therapeutic targets in the treatment of fibrotic diseases.
70 tissues might be used to treat patients with fibrotic diseases.
71 cal mechanisms involved in wound healing and fibrotic diseases.
72 rotein response (UPR) in the pathogenesis of fibrotic diseases.
73 flexor tendons and other tissues as well as fibrotic diseases.
74 l therapeutic targets in inflammation-driven fibrotic diseases.
75 l therapeutic approach in treating pulmonary fibrotic diseases.
76 promising new therapeutic approach for human fibrotic diseases.
77 action may be useful in treating a number of fibrotic diseases.
78 on by fibroblasts contributes to scarring in fibrotic diseases.
79 of modifying the deleterious effects of the fibrotic diseases.
80 gnature" that can be used as a biomarker for fibrotic diseases.
81 ent pose an enormous challenge when treating fibrotic diseases.
82 ch with broad applicability in oncologic and fibrotic diseases.
84 fferences, it was assumed that the different fibrotic diseases also have different pathomechanisms.
85 ticulum (ER) stress is an emerging factor in fibrotic disease, although precise mechanisms are not cl
90 fate of myofibroblasts in various important fibrotic diseases and describe how manipulation of macro
91 iven that TGF-beta has been shown to promote fibrotic diseases and desmoplasia, identifying the fibro
94 tive and novel approach for the treatment of fibrotic diseases and modulation of profibrogenic effect
96 en the link between TGF-beta1 expression and fibrotic disease, and demonstrate the potency of TGF-bet
101 The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibro
104 Interleukin 13 (IL-13) is a key factor in fibrotic disease associated with helminth infection, but
105 being developed for schistosomiasis or other fibrotic diseases associated with a T-helper 2 cell-medi
106 critical driver of collagen accumulation and fibrotic disease but also a vital suppressor of inflamma
107 s a potential therapy for cardiovascular and fibrotic diseases, but its short in vivo half-life is an
108 critical event in the pathogenesis of human fibrotic diseases, but regulatory mechanisms for this ef
109 drome, lung adenocarcinoma, and debilitating fibrotic diseases, but the critical transcription factor
110 aling through one of its receptors, LPA1, in fibrotic diseases, but the mechanisms by which LPA-LPA1
111 lungs and contribute to remodelling in other fibrotic diseases, but their involvement in allergic ast
112 ic target for a number of diseases including fibrotic diseases, cancer, and inflammation, among other
113 thway will be highly effective at preventing fibrotic disease caused by chronic Th2-mediated inflamma
115 ay be important in the pathogenesis of human fibrotic diseases characterized by overexpression/activa
116 and more effective therapeutic strategy for fibrotic diseases characterized by persistent myofibrobl
117 SMAD7 has been reported in TGF-beta-mediated fibrotic diseases, characterized by overproduction of co
118 rogression, tumorigenesis, neuropathic pain, fibrotic diseases, cholestatic pruritus, lymphocyte homi
120 GF-beta1, a central pathological mediator of fibrotic diseases, enhanced miR-21 expression in primary
121 c approach to treating scleroderma and other fibrotic diseases finds support in animal studies and an
124 in increased numbers in a variety of chronic fibrotic diseases; however, their role in the developmen
125 olved in the pathogenesis of a proto-typical fibrotic disease, idiopathic pulmonary fibrosis (IPF).
126 in the design of therapeutic modalities for fibrotic disease in the cornea and other parts of the ey
127 and MSC-like cells in myofibroblast-mediated fibrotic disease in the kidney, lung, heart, liver, skin
128 enchymal transition (EMT) is associated with fibrotic diseases in the lens, such as anterior subcapsu
130 lasminogen activation system on TGF-beta1 in fibrotic diseases in vivo, as well as novel prognostic a
131 n signaling, a pathway implicated in several fibrotic diseases, in RPE cells in proliferative vitreor
132 TGFbeta has been implicated in promoting fibrotic diseases including CR, but is beneficial in the
134 licated in aberrant fibroblast activation in fibrotic diseases including systemic sclerosis (SSc).
136 TGF-beta has an established role in many fibrotic diseases, including glomerulosclerosis, where i
138 Here, we demonstrate that many endstage fibrotic diseases, including IPF; scleroderma; myelofibr
139 role in the pathogenesis of inflammatory and fibrotic diseases, including radiation-induced fibrosis.
140 extracellular matrix is the hallmark of many fibrotic diseases, including systemic sclerosis and pulm
141 g angiogenesis, autoimmune diseases, cancer, fibrotic diseases, inflammation, neurodegeneration, and
146 plasminogen activator inhibitor-1 (PAI-1) in fibrotic diseases is well documented, its role in cardia
147 (CTGF/CCN2), associated with multiple human fibrotic diseases, is overexpressed in the tissue of gin
149 IL-13) in systemic sclerosis (SSc) and other fibrotic diseases, its mechanisms of action are not unde
150 urthermore, these mechanisms are involved in fibrotic disease itself, with some miRs and epigenetic d
152 gments in the plasma of patients with severe fibrotic disease may be a product of CTGF proteolysis th
153 llowing lens injury and were responsible for fibrotic disease of the lens that occurs following catar
154 ulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology.
155 Idiopathic pulmonary fibrosis (IPF) is a fibrotic disease of unknown etiology that results in sig
156 tractional force is a contributing factor to fibrotic diseases of the eye, such as proliferative vitr
162 en FSR correlates with established risks for fibrotic disease progression in NASH, and plasma lumican
163 o monitor the contribution of macrophages to fibrotic disease progression in the bleomycin-induced mu
165 ensing process in complex tissues, including fibrotic disease states with high collagen, is now utili
166 nective tissue growth factor is expressed in fibrotic disease such as scleroderma, where it is believ
167 is a prominent feature of chronic pulmonary fibrotic diseases such as idiopathic interstitial pneumo
168 ta promotes excessive collagen deposition in fibrotic diseases such as idiopathic pulmonary fibrosis
169 plicated in the deposition of ECM protein in fibrotic diseases such as pulmonary fibrosis and atheros
173 wounds, in the stroma of some tumors, and in fibrotic diseases such as systemic sclerosis (SSc) and r
175 in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary fibrosis
176 in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary fibrosis
178 urrent bleak outlook for chronic progressive fibrotic diseases, such as scleroderma, due to lack of e
179 hibitory effects of sST2 in inflammatory and fibrotic diseases, suggesting that IL-33/ST2 is a unique
181 ta has emerged as central effector of MD and fibrotic disease, the cell types in diseased muscle that
183 ugh it has not been previously implicated in fibrotic disease, we found that Dril1 was highly express
184 ixed connective tissue disease, two systemic fibrotic diseases, were less able to inhibit fibrocyte d
185 ne the role of PI3K activation in human lung fibrotic disease, which could be amenable to targeted th
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