ライフサイエンスコーパス: pathological angiogenesis

1 th factor (VEGF) is essential for normal and pathological angiogenesis.

2 a-3-PUFA or their bioactive products reduces pathological angiogenesis.

3 or (VEGF) is essential for developmental and pathological angiogenesis.

4 is integrity during vascular development and pathological angiogenesis.

5 ights into the role of integrin-VEGF axis in pathological angiogenesis.

6 ies consistent with a role during normal and pathological angiogenesis.

7 scular permeability during physiological and pathological angiogenesis.

8 may provide a useful target for reduction of pathological angiogenesis.

9 y identify new molecular targets to regulate pathological angiogenesis.

10 s of Akt1 knockout on vascular integrity and pathological angiogenesis.

11 tant implications for both physiological and pathological angiogenesis.

12 ds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis.

13 ifunctional cytokine with important roles in pathological angiogenesis.

14 osine kinase that mediates physiological and pathological angiogenesis.

15 play an important role in physiological and pathological angiogenesis.

16 by TN-C suggest a potential role for TN-C in pathological angiogenesis.

17 nt in high VEGF conditions, as occurs during pathological angiogenesis.

18 in vasculogenesis and both physiological and pathological angiogenesis.

19 which plays an important role in normal and pathological angiogenesis.

20 nd regression of conditions characterized by pathological angiogenesis.

21 ) plays important roles in physiological and pathological angiogenesis.

22 DR play important roles in physiological and pathological angiogenesis.

23 ossibility of a novel approach to inhibiting pathological angiogenesis.

24 ptosis is a critical modulator of normal and pathological angiogenesis.

25 nd plays a key role during physiological and pathological angiogenesis.

26 Flt-1, play a key role in physiological and pathological angiogenesis.

27 growth factor (VEGF) is a major mediator of pathological angiogenesis.

28 , with direct relevance to physiological and pathological angiogenesis.

29 ted through a negative-feedback loop driving pathological angiogenesis.

30 ring novel therapeutic strategies to control pathological angiogenesis.

31 ent to maintain vascular homeostasis but not pathological angiogenesis.

32 signaling and contributes to the process of pathological angiogenesis.

33 ication signals in driving physiological and pathological angiogenesis.

34 l posttranscriptional mechanism critical for pathological angiogenesis.

35 by exacerbating STAT3 activation, leading to pathological angiogenesis.

36 s, thereby linking atherogenic processes and pathological angiogenesis.

37 major driver of solid tumor progression and pathological angiogenesis.

38 ributing to retinal vascular dysfunction and pathological angiogenesis.

39 ntial therapeutic target in the treatment of pathological angiogenesis.

40 sm EGFL7 engages to govern physiological and pathological angiogenesis.

41 ression of the IGFBP-vWC variant exacerbated pathological angiogenesis.

42 d to play an important role in embryonic and pathological angiogenesis.

43 n essential role in vascular development and pathological angiogenesis.

44 bute to more effective strategies to control pathological angiogenesis.

45 ould offer a new target for the treatment of pathological angiogenesis.

46 erapeutic agents that are more selective for pathological angiogenesis.

47 een shown to regulate both physiological and pathological angiogenesis.

48 targeting may allow selective inhibition of pathological angiogenesis.

49 hairpin RNAs had no effect on the extent of pathological angiogenesis.

50 -C may provide a novel route for controlling pathological angiogenesis.

51 we studied the involvement of complement in pathological angiogenesis.

52 A) is a major regulator of physiological and pathological angiogenesis.

53 LXA(4) circuit as an endogenous regulator of pathological angiogenesis.

54 apparently distinct for physiological versus pathological angiogenesis.

55 rophin (PTN, Ptn) stimulates both normal and pathological angiogenesis.

56 giogenesis and block its activity to control pathological angiogenesis.

57 profile of VEGF-B in both physiological and pathological angiogenesis, a neutralising anti-VEGF-B an

58 t the actions of these inhibitors to promote pathological angiogenesis, a requisite event for tumor p

59 During physiological and pathological angiogenesis, AGM is upregulated in the ang

60 Pathological angiogenesis also occurs in the retina and

61 trikingly reduced in cav-1(-/-) mice, as was pathological angiogenesis and associated chronic vascula

62 r hyperpermeability induced by VEGF-A and in pathological angiogenesis and associated chronic vascula

63 gulate inflammation and foam cell formation, pathological angiogenesis and calcification, which are c

64 angiogenic gene expression, which suppresses pathological angiogenesis and CNV development.

65 re not essential for vascular development or pathological angiogenesis and highlight the need for fur

66 n-1 regulates portal hypertension-associated pathological angiogenesis and highlights that increasing

67 endothelial alpha3beta1 negatively regulates pathological angiogenesis and implicate an unexpected ro

68 vessels arising from disease states such as pathological angiogenesis and inflammatory response.

69 n N-terminal kinase 1 (JNK1) exhibit reduced pathological angiogenesis and lower levels of retinal VE

70 nt role in developmental, physiological, and pathological angiogenesis and lymphangiogenesis.

71 actor (VEGF) exerts crucial functions during pathological angiogenesis and normal physiology.

72 thesized that EPOR signaling is important in pathological angiogenesis and tested this hypothesis usi

73 elial cells and in several in vivo models of pathological angiogenesis and that different from DSCR1-

74 can be further explored to modulate both the pathological angiogenesis and the tumorigenesis.

75 The role of PDGF-DD in pathological angiogenesis and the underlying cellular an

76 elin system via EDNRA plays a causal role in pathological angiogenesis and up-regulation of angiogeni

77 helial cells and retinal pericytes to induce pathological angiogenesis and vascular remodeling during

78 stasis and disease processes such as cancer, pathological angiogenesis, and inflammation through two

79 t PDGF-DD expression was up-regulated during pathological angiogenesis, and inhibition of PDGF-DD sup

80 odify Eph signaling in therapies for cancer, pathological angiogenesis, and nerve regeneration.

81 evidence suggests that hepatic fibrosis and pathological angiogenesis are interdependent processes t

82 se this endothelial quiescence to facilitate pathological angiogenesis are not yet completely underst

83 Pathological angiogenesis, as seen in many inflammatory,

84 ide a useful therapeutic approach to control pathological angiogenesis associated with HSV induced st

85 ether this cytokine could play a role in the pathological angiogenesis associated with human diseases

86 VEGF has also been implicated in pathological angiogenesis associated with tumors, intrao

87 Pathological angiogenesis associated with wound healing

88 culogenesis during embryonic development and pathological angiogenesis, but little is known about the

89 /tissue barrier dysfunctions associated with pathological angiogenesis, but the mechanisms of VEGF-in

90 ble microRNA in the endothelium, facilitates pathological angiogenesis by downregulating p120RasGAP,

91 e that PlGF-containing ligands contribute to pathological angiogenesis by prolonging cell survival si

92 trocytoma, we report that tumor cells induce pathological angiogenesis by suppressing expression of t

93 1, or canonical TGFbeta receptors results in pathological angiogenesis caused by defective neuroepith

94 a master regulator of both developmental and pathological angiogenesis, composed of an oxygen-sensiti

95 Pathological angiogenesis contributes directly to profou

96 Pathological angiogenesis contributes to various ocular,

97 on between the DNA damage repair pathway and pathological angiogenesis could open previously unexplor

98 can be selectively targeted during states of pathological angiogenesis, despite its ubiquitous distri

99 bbing in LEC and thereby drives invasion and pathological angiogenesis during cirrhosis.

100 fibrosis; however, the pathways controlling pathological angiogenesis during lung disease are not co

101 Added to the complexity is the occurrence of pathological angiogenesis during the course of disease p

102 focally and intensely expressed at sites of pathological angiogenesis (e.g. tumor vasculature).

103 retinal vasculature to hyperoxia and reduced pathological angiogenesis following ischemia.

104 Pathological angiogenesis has a pivotal role in sustaini

105 unction, no previous bioelectric analysis of pathological angiogenesis has been reported.

106 (VEGF)-A as a major regulator of normal and pathological angiogenesis has enabled significant progre

107 Moreover, miR-23 and miR-27 are required for pathological angiogenesis in a laser-induced choroidal n

108 ology tools, we show that EYA contributes to pathological angiogenesis in a model of oxygen-induced r

109 Finally, loss of MAP4K4 function suppressed pathological angiogenesis in disease models, identifying

110 In contrast, pathological angiogenesis in experimental tumors was alt

111 ely linked, and their dysregulation leads to pathological angiogenesis in human diseases.

112 tly promotes endothelial cell activation and pathological angiogenesis in our previous study, but the

113 helial cell glycolysis, which is crucial for pathological angiogenesis in proliferative retinopathies

114 Pathological angiogenesis in the eye is an important fea

115 ) in retinas at postnatal day 18 (p18), when pathological angiogenesis in the form of intravitreal ne

116 RhoB null mice, that loss of RhoB decreases pathological angiogenesis in the ischaemic retina and re

117 hors show that adenosine receptor A2A drives pathological angiogenesis in the oxygen-induced retinopa

118 -KO)) results in defective physiological and pathological angiogenesis in the postnatal retina and tu

119 Pathological angiogenesis in the retina is driven by dys

120 nnective tissue growth factor (CTGF/CCN2) in pathological angiogenesis in the retina is unknown.

121 Accordingly, both physiological and pathological angiogenesis in the retina were inhibited b

122 The alternative complement pathway regulates pathological angiogenesis in the retina.

123 e, EPO is involved in both physiological and pathological angiogenesis in the retina.

124 tential novel therapeutic approach to target pathological angiogenesis in these conditions would be t

125 We demonstrate that resveratrol can inhibit pathological angiogenesis in vivo and in vitro by a sirt

126 motility and vascular assembly in vitro and pathological angiogenesis in vivo, thereby inhibiting tu

127 pressed in several types of VEGF-A-dependent pathological angiogenesis in vivo.

128 an important positive role in the process of pathological angiogenesis in vivo.

129 nd is equally required for developmental and pathological angiogenesis, including during tumor growth

130 of human cancer and related disorders where pathological angiogenesis is a component.

131 Pathological angiogenesis is a major cause of vision los

132 poorly understood clinical manifestation of pathological angiogenesis is angiodysplasia, vascular ma

133 Pathological angiogenesis is associated with disease sta

134 of identifying VEGF-independent pathways in pathological angiogenesis is increasingly recognized as

135 In adults, physiological or pathological angiogenesis is initiated by tissue demands

136 treatment of cancer and other diseases where pathological angiogenesis is involved.

137 A role for fibroblasts in physiological and pathological angiogenesis is now well recognized; howeve

138 Because only pathological angiogenesis is sensitive to decreased leve

139 agonists in patients for which inhibition of pathological angiogenesis is the therapeutic goal.

140 al growth factor (VEGF) in developmental and pathological angiogenesis is well established, its funct

141 been well studied in both developmental and pathological angiogenesis, its role in mature blood vess

142 Intriguingly, in contrast to reducing pathological angiogenesis, lack of MMP-12 accelerated re

143 -126), physiological (miR-126, miR-92a), and pathological angiogenesis (miR-200b, miR-132).

144 e, the hyperpermeable blood vessels found in pathological angiogenesis, mother vessels, are derived f

145 Pathological angiogenesis occurs in hepatocellular carci

146 In pathological angiogenesis of human ovarian carcinomas, r

147 normal vascularization and hypoxia-triggered pathological angiogenesis of the mouse retina.

148 anisms that serve to couple tumor hypoxia to pathological angiogenesis, our findings provide novel op

149 etinopathies and other diseases dependent on pathological angiogenesis.Pathological angiogenesis in t

150 with retinopathy or other diseases in which pathological angiogenesis plays a significant role.

151 Pathological angiogenesis represents a critical hallmark

152 Two distinct models of pathological angiogenesis revealed that neovascularizati

153 els has a protective role as an inhibitor of pathological angiogenesis, such as choroidal neovascular

154 ical angiogenesis and is a major mediator of pathological angiogenesis, such as tumor-associated neov

155 ot only on multiple cell types important for pathological angiogenesis, such as vascular mural and en

156 ery lesions, supporting its association with pathological angiogenesis suggested by our in vitro resu

157 opathy and a repressive function of let-7 in pathological angiogenesis, suggesting distinct implicati

158 ormal embryonic angiogenesis and also in the pathological angiogenesis that occurs in a number of dis

159 critical in designing targeted inhibitors of pathological angiogenesis that underlies cancer and othe

160 Pathological angiogenesis, the development of a microvas

161 Inhibiting pathological angiogenesis therefore represents a promisi

162 dependent inflammation leads to ischemia and pathological angiogenesis through Semaphorin 3A.

163 role in neuronal outgrowth and developmental/pathological angiogenesis via interactions with netrin-1

164 lecules exert a feedback control to restrain pathological angiogenesis, which includes physical bindi

165 To evaluate the role of ESAM in pathological angiogenesis, wild type (WT) and ESAM-/- mi

166 rapeutic strategies that specifically target pathological angiogenesis without affecting physiologica