ライフサイエンスコーパス: renal ischemia

1 t in the prevention or treatment of AKI from renal ischemia.

2 reserving kidney function during episodes of renal ischemia.

3 tive period, the most common cause of AKI is renal ischemia.

4 lar injury and organ dysfunction after acute renal ischemia.

5 iption of TNF-alpha and MCP-1 in response to renal ischemia.

6 MCP-1 by the proximal tubule in response to renal ischemia.

7 that are capable of mobilizing EPCs in acute renal ischemia.

8 therapeutic strategies for renal tumors and renal ischemia.

9 hat distant lung injury occurs rapidly after renal ischemia.

10 ue-Dawley rats after 45 minutes of bilateral renal ischemia.

11 g injury develops after shock or visceral or renal ischemia.

12 s recently been reported to be induced after renal ischemia.

13 bradykinin, methacholine, or morphine before renal ischemia.

14 a, and inner medulla of rats after bilateral renal ischemia.

15 nhibits renal injury in a model of bilateral renal ischemia.

16 y the patterns of NOS activity in a model of renal ischemia.

17 ted acute renal failure in rats subjected to renal ischemia.

18 in the development of tubular obstruction in renal ischemia.

19 e 2 mg/kg dose of OKY-046 administered after renal ischemia.

20 rom the injury and mortality associated with renal ischemia.

21 ro-ischemia technique that eliminates global renal ischemia.

22 njury and improved kidney function following renal ischemia.

23 his system is profoundly perturbed following renal ischemia, a leading cause of acute kidney injury (

24 panies renal ischemia, it is unknown whether renal ischemia affects the production of antibodies by B

25 induction of ischemia in the mouse model of renal ischemia, an increase in intrarenal expression of

26 Rats were subjected to 60 min of bilateral renal ischemia and 6 h of reperfusion in the absence or

27 n results in pulmonary injury independent of renal ischemia and highlight the critical role of the ki

28 mobilized into the circulation by transient renal ischemia and home specifically to injured regions

29 osatetraenoic acid levels are elevated after renal ischemia and may protect against injury.

30 rine was related to the dose and duration of renal ischemia and preceded the appearance of other urin

31 ith SS-31 protected cristae membranes during renal ischemia and prevented mitochondrial swelling.

32 Cytoskeletal degradation occurs in warm renal ischemia and reperfusion and during hypothermia.

33 Renal ischemia and reperfusion injury causes loss of ren

34 trite anions may play a role in normothermic renal ischemia and reperfusion.

35 dergo a change in activity or function after renal ischemia and reperfusion.

36 a levels in Adora2b-deficient mice following renal ischemia and reperfusion.

37 7 on parenchymal cells promotes injury after renal ischemia and reperfusion.

38 f alpha-MSH inhibits acute lung injury after renal ischemia and to determine the early mechanisms of

39 Here, we developed a series of murine renal ischemia and transplant models to investigate sex-

40 A), or right nephrectomy with 60 min of left renal ischemia and treatment with inactive vehicle only

41 18 (mild IRI) or 22 min (moderate IRI) warm renal ischemia, and analyzed 24 h after reperfusion for

42 on animal survival after transient bilateral renal ischemia associated with severe AKI.

43 significant renal failure), suggesting that renal ischemia but not uremia is necessary for the apopt

44 lpha and that administration of xenon before renal ischemia can prevent acute renal failure.

45 erol did not raise hepatic FC/CE; unilateral renal ischemia did not alter contralateral renal FC/CE l

46 this procedure laparoscopically, namely warm renal ischemia during occlusion of the renal vascular pe

47 hemia and reperfusion) and then to 30 min of renal ischemia either 15 min (acute IPC) or 24 h (delaye

48 When rats were subjected to 45 min of renal ischemia, electrophoretic mobility shift assays of

49 Acute renal ischemia elicits an inflammatory response that may

50 y can now be safely performed without global renal ischemia, even for complex tumors.

51 Rats recovering from acute renal ischemia exhibit tubule loss and interstitial fibr

52 nsgenic mice were subjected to 26 minutes of renal ischemia followed by reperfusion for 72 hours.

53 on from IRI induced by 27.5 min of bilateral renal ischemia, followed by 20 h of reperfusion (blood u

54 57BL/6), ARF was induced by 32 min bilateral renal ischemia, followed by reperfusion (I/R).

55 erexpressing (HBAC) mice underwent bilateral renal ischemia for 10 minutes.

56 Twenty-four hours after bilateral renal ischemia for 22.5 minutes, transgenic sickle mice

57 to male Wistar rats 30 min before bilateral renal ischemia for 45 min followed by reperfusion for up

58 s of the brain in mice by inducing bilateral renal ischemia for 60 min and studying the brains 24 h l

59 d-type and Adora2b-deficient mice undergoing renal ischemia for expression of a range of inflammatory

60 the hypothesis that cytokines released with renal ischemia have effects on other organ systems.

61 We examined the effect of renal ischemia in a transgenic mouse expressing human si

62 abbits (3.1-3.5 kg), with experimental focal renal ischemia in five kidneys.

63 nistered intravenously 24 and 48 hours after renal ischemia in rats.

64 APRF was induced by bilateral renal ischemia in situ (32 min), followed by reperfusion

65 a (TNF-alpha) and interleukin-1 (IL-1) after renal ischemia in the mouse.

66 olecule-1 mRNA were found in the heart after renal ischemia in the rat.

67 Thus, renal ischemia in this murine model induces more severe

68 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in c

69 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in N

70 study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in T

71 ts against both kidney and lung damage after renal ischemia, in part, by inhibiting activation of tra

72 Functional changes in the heart 48 h after renal ischemia included increases in left ventricular en

73 Notably, renal ischemia induced a transient increase in cellular

74 Transient renal ischemia induces both inflammatory and fibrotic pr

75 This study documents that renal ischemia induces dynamic changes in the molecular

76 vivo rat ischemic model to demonstrate that renal ischemia induces podocyte effacement with loss of

77 e assessed for delayed complications such as renal ischemia, infarct, urinoma, or tumor recurrence.

78 so found 48 h after an abbreviated period of renal ischemia insufficient to induce azotemia but not b

79 Renal ischemia is among the leading causes of acute kidn

80 Because renal ischemia is characterized by disruption of the ren

81 Renal ischemia is the result of a complex series of even

82 Global renal ischemia is thus eliminated.

83 nce of renal vasoconstriction and subsequent renal ischemia, is a common problem for which no proven

84 s known that tissue inflammation accompanies renal ischemia, it is unknown whether renal ischemia aff

85 Bilateral renal ischemia led to the expiration of 64% of wild-type

86 of chronic allograft nephropathy by causing renal ischemia mediated by vasoconstrictive metabolites

87 tected against the heightened sensitivity to renal ischemia observed in sickle mice, preventing ische

88 With bilateral renal ischemia of greater duration (22.5 minutes), and a

89 With bilateral renal ischemia of short or long duration, renal expressi

90 In AS160-knockout mice, the effects of renal ischemia on the distribution of Na(+),K(+)-ATPase

91 Mice subjected to renal ischemia or bilateral nephrectomy had moderate to

92 Mice underwent 32-min bilateral renal ischemia or identical sham operations.

93 studied 24 and 72 hours after 30 minutes of renal ischemia or sham operation.

94 subjected to 30 minutes of either unilateral renal ischemia or sham surgery.

95 Renal ischemia or the loss of blood flow to the kidneys

96 The impact of 40 minutes of unilateral renal ischemia plus reflow (3 to 6 days) on mouse cortic

97 cted into wild-type C57BL/6 mice 24 h before renal ischemia, protect mice from developing renal IRI.

98 Renal ischemia rapidly activated kidney and lung nuclear

99 gher in renalase-deficient mice subjected to renal ischemia reperfusion compared with wild-type mice.

100 Renal ischemia reperfusion injury (IRI) is associated wi

101 have been implicated in the pathogenesis of renal ischemia reperfusion injury (IRI).

102 role for CD4(+) cells in the pathogenesis of renal ischemia reperfusion injury (IRI).

103 loss of function in the absence of IgM after renal ischemia reperfusion injury and cardiac allograft

104 Here, mice subjected to renal ischemia reperfusion injury had significantly lowe

105 Renal ischemia reperfusion injury triggers complement ac

106 The protective effect on renal ischemia reperfusion injury was not observed using

107 ded to further examine the effects of HMP on renal ischemia reperfusion injury.

108 e in rabbits, and there were too few data on renal ischemia reperfusion injury.

109 asma NE levels increased significantly after renal ischemia reperfusion injury.

110 osis, suggesting that it may protect against renal ischemia reperfusion injury.

111 en investigated in cerebral, myocardial, and renal ischemia reperfusion injury; helium and xenon have

112 In a study of renal ischemia reperfusion, cysteamine therapy initiated

113 ith broad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice.

114 BACKGROUND Following allotransplantation, renal ischemia-reperfusion (I/R) injury initiates a seri

115 nized to be important in the pathogenesis of renal ischemia-reperfusion (I/R) injury.

116 l cell (EC) activation plays a major role in renal ischemia-reperfusion (I/R) injury.

117 Renal ischemia-reperfusion (I/R) is a major contributor

118 BL/6 mice were subjected to 30 min bilateral renal ischemia-reperfusion (I/R) to induce AKI.

119 sphate receptor 1 (S1P(1)R) protects against renal ischemia-reperfusion (IR) injury and inflammation,

120 of wild-type mice with retinoic acid before renal ischemia-reperfusion blunted the induction of Nur7

121 Renal ischemia-reperfusion caused a rapid decrease in se

122 tophagy was induced in kidney tissues during renal ischemia-reperfusion in mice.

123 e pharmacologic strategy proposed to prevent renal ischemia-reperfusion injuries and delayed graft fu

124 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with

125 d during the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague

126 plement regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models,

127 Renal ischemia-reperfusion injury (IRI) is a feature of

128 However, its role in renal ischemia-reperfusion injury (IRI) is controversial

129 Renal ischemia-reperfusion injury (IRI) leads to acute k

130 To examine the role of the inflammasome in renal ischemia-reperfusion injury (IRI) we also tested i

131 s (Tregs) can suppress immunologic damage in renal ischemia-reperfusion injury (IRI), but the isolati

132 , these animals were remarkably resistant to renal ischemia-reperfusion injury (IRI), showing signifi

133 renal protective effect of A(2A) agonists in renal ischemia-reperfusion injury (IRI).

134 tream from protein kinase C (PKC) may reduce renal ischemia-reperfusion injury and confer renal graft

135 assessed in the kidneys of 6 mice undergoing renal ischemia-reperfusion injury and in 6 control kidne

136 trin-1 acting through UNC5B receptor reduces renal ischemia-reperfusion injury and its associated ren

137 es acute renal failure, and the hallmarks of renal ischemia-reperfusion injury are inflammation, apop

138 Renal ischemia-reperfusion injury causes acute renal fai

139 In an established mouse model of renal ischemia-reperfusion injury characterized by apopt

140 zed with a foreign antigen 24-96 hours after renal ischemia-reperfusion injury developed increased le

141 Renal ischemia-reperfusion injury did not cause amplific

142 that dehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats.

143 ce renal IL-11 expression or protect against renal ischemia-reperfusion injury in mice lacking the re

144 inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo.

145 Pretreatment with CCPA protected against renal ischemia-reperfusion injury in wild-type mice, but

146 Renal ischemia-reperfusion injury induced hepatosplenic

147 Renal ischemia-reperfusion injury is mediated by a compl

148 Results of this study in a renal ischemia-reperfusion injury model allow phenotype

149 ive effect of amniotic fluid stem cells in a renal ischemia-reperfusion injury model.

150 d a mouse model to investigate the effect of renal ischemia-reperfusion injury on systemic iron homeo

151 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and

152 In summary, renal ischemia-reperfusion injury results in profound al

153 s an endogenous protective mechanism against renal ischemia-reperfusion injury through inhibition of

154 lar injury in kidneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the

155 Renal ischemia-reperfusion injury with bilateral renal p

156 Six hours after induction of renal ischemia-reperfusion injury, amniotic fluid stem c

157 reduced netrin-1-mediated protection against renal ischemia-reperfusion injury, and it increased mono

158 rophages rapidly infiltrate the kidney after renal ischemia-reperfusion injury, however specific mole

159 nd neutrophils to kidney in a mouse model of renal ischemia-reperfusion injury, however this activity

160 In an established murine model of renal ischemia-reperfusion injury, intravenous NGAL admi

161 human amniotic fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic,

162 After renal ischemia-reperfusion injury, MFG-E8 mRNA and prote

163 ing in plasma samples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to ren

164 a nitrogen and serum creatinine in rats with renal ischemia-reperfusion injury, providing evidence fo

165 educes inflammation to mediate protection in renal ischemia-reperfusion injury, suggesting that hepci

166 In a mouse model of renal ischemia-reperfusion injury, tempol-folate reduced

167 ion, although both C3a and C5a contribute to renal ischemia-reperfusion injury, the pathogenic role o

168 -, or C3aR/C5aR-deficient mice and models of renal ischemia-reperfusion injury, we found that deficie

169 Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 p

170 In a model of renal ischemia-reperfusion injury, xenon provided morpho

171 econditional HIF activation protects against renal ischemia-reperfusion injury, yet the mechanisms in

172 ce, systemic iron overload protected against renal ischemia-reperfusion injury-associated sterile inf

173 G-E8 can be developed as novel treatment for renal ischemia-reperfusion injury.

174 whether administration of MFG-E8 attenuates renal ischemia-reperfusion injury.

175 nd the inflammatory response after sublethal renal ischemia-reperfusion injury.

176 ophil infiltration in a 7 day mouse model of renal ischemia-reperfusion injury.

177 subjected hif1a(+/-) and hif2a(+/-) mice to renal ischemia-reperfusion injury.

178 eptor shown to contribute to fibrogenesis in renal ischemia-reperfusion injury.

179 n uninjured kidney or intra-arterially after renal ischemia-reperfusion injury.

180 , mediated by C1 neurons: protection against renal ischemia-reperfusion injury.

181 3 hours) treatment with necrostatin-1 during renal ischemia-reperfusion injury.

182 f talin-mediated activation of integrins for renal ischemia-reperfusion injury.

183 stress is implicated in the pathogenesis of renal ischemia-reperfusion injury.

184 ies is a major cause of tissue damage during renal ischemia-reperfusion injury.

185 alpha12 activation and protects mice against renal ischemia-reperfusion injury.

186 (L325R) in myeloid cells were protected from renal ischemia-reperfusion injury.

187 eukocytes contributes to the pathogenesis of renal ischemia-reperfusion injury.

188 l cells or circulating leukocytes attenuated renal ischemia-reperfusion injury.

189 After induction of AKI in mice by renal ischemia-reperfusion or bilateral nephrectomy, sma

190 tion of recombinant netrin-1 before or after renal ischemia-reperfusion reduced kidney injury, apopto

191 After renal ischemia-reperfusion, Nurr77-deficient mice exhibi

192 Exogenous hepcidin treatment prevented renal ischemia-reperfusion-induced changes in iron homeo

193 bule-specific deletion of Drp1 prevented the renal ischemia-reperfusion-induced kidney injury, inflam

194 tic benefit in models of ischemic stroke and renal ischemia-reperfusion.

195 eness in the setting of preceding unilateral renal ischemia/reperfusion (I/R) in mouse AKI model.

196 Renal ischemia/reperfusion (I/R) injury is a major cause

197 cohydrolase (PARG) in the pathophysiology of renal ischemia/reperfusion (I/R) injury is not known.

198 ium nitrite administration in a rat model of renal ischemia/reperfusion (I/R) injury.

199 ctivated within the tubulointerstitium after renal ischemia/reperfusion (I/R).

200 ge of mitochondria in experimental models of renal ischemia/reperfusion and cisplatin-induced nephrot

201 red in proximal tubular cells in mice during renal ischemia/reperfusion and cisplatin-induced nephrot

202 ess the role of Nlrp3 in the repair phase of renal ischemia/reperfusion and investigate the relative

203 rate of epithelial cell proliferation after renal ischemia/reperfusion in aged mice but also increas

204 owever, the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully de

205 at polyclonal natural IgM protects mice from renal ischemia/reperfusion injury (IRI) by inhibiting th

206 s poorly defined, the role of cathepsin G in renal ischemia/reperfusion injury was tested.

207 by chloroquine and 3-methyladenine worsened renal ischemia/reperfusion injury, as indicated by renal

208 se results suggest that CSE protects against renal ischemia/reperfusion injury, likely by modulating

209 ctional kidney changes, and mortality during renal ischemia/reperfusion injury.

210 ssue pathology and subsequent fibrosis after renal ischemia/reperfusion injury.

211 ed with increased damage and mortality after renal ischemia/reperfusion injury.

212 ole for Galpha12 activation during bilateral renal ischemia/reperfusion injury.

213 We conclude: (a) alpha-MSH protects against renal ischemia/reperfusion injury; and (b) it may act, i

214 Renal ischemia/reperfusion is a major cause of acute kid

215 chemotactic protein-1, and P-selectin, after renal ischemia/reperfusion, exacerbating apoptosis and f

216 osis factor-alpha at early time points after renal ischemia/reperfusion.

217 he alternative splicing during the course of renal ischemia/reperfusion.

218 ice from death and hypothermia in sepsis and renal ischemia/reperfusion.

219 l artery contraction by AT1R activation with renal ischemia representing a key permissive factor and

220 allin in various renal compartments; and (2) Renal ischemia results in differential accumulation of h

221 Renal ischemia results in distant effects and the altera

222 Examination of graded times of renal ischemia revealed a direct correlation between the

223 ed, FVB/NJ mice that were subjected to acute renal ischemia showed a transient surge in UA level in t

224 Thirty minutes of renal ischemia significantly elevated serum creatinine i

225 maintaining blood flow during recovery from renal ischemia, the observed decrease in NOS activity ma

226 During the repair phase of transient renal ischemia, these cells entered the cell cycle and t

227 Mice were subjected to renal ischemia treated with vehicle or alpha-MSH.

228 IL-6 that was produced in response to renal ischemia was maladaptive because transgenic knocko

229 Three days later, renal ischemia was produced by cross-clamping the left r

230 present study, an animal model of bilateral renal ischemia was used to test the hypothesis that cyto

231 ion of metabolic stress, which occurs during renal ischemia, we infected immortalized and primary pro

232 factors are simultaneously activated during renal ischemia, which might account for observed differe

233 a greater rise in blood urea nitrogen after renal ischemia, while stem cell infusion after bone marr

234 enal genes that are induced very early after renal ischemia, whose protein products might serve as no

235 6), consisting of 3 cycles of 30 seconds of renal ischemia with 30 seconds intervening reperfusion.

236 C57BL/6 mice were subjected to 30 min of renal ischemia, with or without pretreatment with 1,3-di