ライフサイエンスコーパス: ischemia-reperfusion injury

1 Young plasma attenuates age-dependent liver ischemia reperfusion injury.

2 ntramyocardial injection in a mouse model of ischemia reperfusion injury.

3 invasive method to protect the heart against ischemia reperfusion injury.

4 ell line cultures using an in vitro model of ischemia reperfusion injury.

5 whereas neon was only explored in myocardial ischemia reperfusion injury.

6 zones of recipient rat hearts 1 month after ischemia reperfusion injury.

7 abbits, and there were too few data on renal ischemia reperfusion injury.

8 unomodulatory properties that could minimize ischemia reperfusion injury.

9 n for decreasing liver damage resulting from ischemia reperfusion injury.

10 for lungs having a shorter CIT due to severe ischemia reperfusion injury.

11 of diseases such as chronic inflammation and ischemia-reperfusion injury.

12 tive MMP-9 inhibition largely abolished warm ischemia-reperfusion injury.

13 nd CD47(-/-) mice were challenged with renal ischemia-reperfusion injury.

14 efficacy of this treatment in reducing early ischemia-reperfusion injury.

15 d higher presence of regulatory T cell after ischemia-reperfusion injury.

16 s) treatment with necrostatin-1 during renal ischemia-reperfusion injury.

17 quently apoptosis in epithelial cells during ischemia-reperfusion injury.

18 ed media and delivered to athymic rats after ischemia-reperfusion injury.

19 sis induced by folic acid (FA) or unilateral ischemia-reperfusion injury.

20 ell (CPC)-derived exosomes in a rat model of ischemia-reperfusion injury.

21 on (tMCAO) model was used to establish brain ischemia-reperfusion injury.

22 inflammatory response after sublethal renal ischemia-reperfusion injury.

23 in mouse models of systemic inflammation and ischemia-reperfusion injury.

24 ated by C1 neurons: protection against renal ischemia-reperfusion injury.

25 the sterile inflammation that follows kidney ischemia-reperfusion injury.

26 at follow intensely loud noise exposures and ischemia-reperfusion injury.

27 tective effects in models of endotoxemia and ischemia-reperfusion injury.

28 investigated in a rodent model of myocardial ischemia-reperfusion injury.

29 ion of sirtuin 1 is protective after hepatic ischemia-reperfusion injury.

30 o play a significant role in mouse models of ischemia-reperfusion injury.

31 vivo models suggest that C1-INH ameliorates ischemia-reperfusion injury.

32 t of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.

33 ic mechanisms involved in the development of ischemia-reperfusion injury.

34 h the transcriptional changes observed after ischemia-reperfusion injury.

35 herapeutic strategy in mitigating myocardial ischemia-reperfusion injury.

36 The pathogenesis of PGD involves ischemia-reperfusion injury.

37 Plexin C1 in a mouse model of early hepatic ischemia-reperfusion injury.

38 ation is restricted by cold preservation and ischemia-reperfusion injury.

39 nd unilateral nephrectomy plus contralateral ischemia-reperfusion injury.

40 evaluate the benefit to patients at risk of ischemia-reperfusion injury.

41 ute coronary occlusion inevitably results in ischemia-reperfusion injury.

42 C1) mice also demonstrated decreased hepatic ischemia-reperfusion injury.

43 y small interfering RNA is effective against ischemia-reperfusion injury.

44 s crucial for reducing the extent of hepatic ischemia-reperfusion injury.

45 p are reported to have a detrimental role in ischemia-reperfusion injury.

46 line, but mRNA and protein are induced after ischemia-reperfusion injury.

47 esponse and improved tissue repair following ischemia-reperfusion injury.

48 c ablation of PHD2 in a mouse model of renal ischemia-reperfusion injury.

49 myocardial fibrosis 28 days post-myocardial ischemia-reperfusion injury.

50 mediator of mitochondrial recovery following ischemia-reperfusion injury.

51 lial immune defense and highly vulnerable to ischemia-reperfusion injury.

52 econditioning in mice before and after renal ischemia-reperfusion injury.

53 schemic stroke infarct volume after cerebral ischemia-reperfusion injury.

54 torage, may better protect these organs from ischemia-reperfusion injury.

55 uloprotective and inhibits cardiac allograft ischemia-reperfusion injury.

56 ssment of cardiac physiology and response to ischemia/reperfusion injury.

57 e neutrophil has a role in murine intestinal ischemia/reperfusion injury.

58 AMPK activity is required to protect against ischemia/reperfusion injury.

59 limb ischemia/reperfusion reduces myocardial ischemia/reperfusion injury.

60 mma2-AMPK sensitizes the heart to myocardial ischemia/reperfusion injury.

61 eurological deficits than sTM after cerebral ischemia/reperfusion injury.

62 ure, electromechanical uncoupling, and acute ischemia/reperfusion injury.

63 nge protein directly activated by cAMP 1) in ischemia/reperfusion injury.

64 the culprit but also a victim of myocardial ischemia/reperfusion injury.

65 gated LPS-mediated protection against kidney ischemia/reperfusion injury.

66 g, anti-inflammatory pathways after cerebral ischemia/reperfusion injury.

67 s, and superior renal function 30 days after ischemia/reperfusion injury.

68 of mitochondrial reactive oxygen species in ischemia/reperfusion injury.

69 ked neuroprotective functions after cerebral ischemia/reperfusion injury.

70 eta15-42 (FX06) has been proven to attenuate ischemia/reperfusion injury.

71 portant pathological mechanism in myocardial ischemia/reperfusion injury.

72 opolysaccharide (LPS) pretreatment on kidney ischemia/reperfusion injury.

73 re and mitophagy is important for mitigating ischemia/reperfusion injury.

74 in cell models and livers of mice undergoing ischemia/reperfusion injury.

75 cyte autophagy, mPTP opening, and death with ischemia/reperfusion injury.

76 is sufficient to decrease infarct size after ischemia/reperfusion injury.

77 oring autoimmunity, and aggravates damage in ischemia/reperfusion injury.

78 tive ultrasound scan, against prolonged cold ischemia-reperfusion injury (24 hours at 4 degrees C), a

79 a protective effect of these noble gases on ischemia reperfusion injury across a broad range of expe

80 The activity of COX contributes to ischemia-reperfusion injury after intestinal transplanta

81 r diseases, including myocardial infarction, ischemia-reperfusion injury after myocardial infarction,

82 Lung ischemia-reperfusion injury after transplantation is ass

83 might be developed to protect patients from ischemia/reperfusion injury after liver surgery or for o

84 and chronic inflammatory diseases, including ischemia/reperfusion injury, allergic asthma, autoimmune

85 ice fully protected the liver against lethal ischemia/reperfusion injury, allowing 100% survival rate

86 Ischemia-reperfusion injury also promoted DC-dependent c

87 Six hours after induction of renal ischemia-reperfusion injury, amniotic fluid stem cells,

88 ysis for argon was only possible in cerebral ischemia reperfusion injury and did not show neuroprotec

89 terventions in vascular inflammation such as ischemia-reperfusion injury and cardiovascular diseases.

90 icrobubble destruction attenuates myocardial ischemia-reperfusion injury and could avoid unwanted sid

91 at the early phase of kidney transplant when ischemia-reperfusion injury and cyclosporin A toxicity m

92 nt cascade as pathogenically contributing to ischemia-reperfusion injury and delayed graft function (

93 essential role in the early phase of hepatic ischemia-reperfusion injury and determine the extent of

94 g syngeneic cardiac transplantation to model ischemia-reperfusion injury and distinguish tissue-resid

95 single dose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function

96 eted hs-MB destruction attenuates myocardial ischemia-reperfusion injury and may avoid unwanted side

97 Tissue necrosis as a consequence of ischemia-reperfusion injury and oxidative damage is a le

98 Cell death is a major component of ischemia-reperfusion injury and posited as the central u

99 impact of exercise on metabolic parameters, ischemia-reperfusion injury and regeneration after hepat

100 mitigates steatosis; however, its impact on ischemia-reperfusion injury and regeneration is unknown.

101 lly distinct donor macrophage populations in ischemia-reperfusion injury and rejection, including the

102 y pharmacological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and

103 rn require a better understanding of cardiac ischemia-reperfusion injury and the various possibilitie

104 inflammatory tissue damage in, for example, ischemia-reperfusion injury and transplant rejection yet

105 m outcome after AKI in two models: bilateral ischemia-reperfusion injury and unilateral nephrectomy p

106 s by peritoneal contamination and infection, ischemia-reperfusion-injury and glycerol-induced acute k

107 b ischemia/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' progno

108 idence of the important role of platelets in ischemia/reperfusion injury and SEC injury.

109 mammalian 'deactive transition' (relevant to ischemia-reperfusion injury) and their effects on the ub

110 splantation field, has shown to reduce liver ischemia-reperfusion injury, and has shown to decrease t

111 cerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in

112 s such as obesity and type 2 diabetes (T2D), ischemia-reperfusion injury, and neurodegenerative disea

113 in the normal kidney and following bilateral ischemia-reperfusion injury, and quantified and compared

114 etic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Plexin C1

115 mice, Bif-1 bound prohibitin-2 during renal ischemia/reperfusion injury, and Bif-1-deficiency protec

116 duces cardiomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac functi

117 bioactivity improved cardiac recovery after ischemia/reperfusion injury, and the response was simila

118 The mechanisms that drive ischemia/reperfusion injury are not well understood; cur

119 and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the levels o

120 ces Keap1/Nrf2 signaling in mice with UUO or ischemia/reperfusion injury, as well as in cultured huma

121 stemic iron overload protected against renal ischemia-reperfusion injury-associated sterile inflammat

122 upregulated within a few hours of bilateral ischemia-reperfusion injury at these sites and new sites

123 stly, proximal tubule deletion of DRP1 after ischemia-reperfusion injury attenuated progressive kidne

124 Administration of C31 in mice with ischemia/reperfusion injury before and during reperfusio

125 drial rupture and cardiomyocyte death during ischemia-reperfusion injury by inducing mitochondrial pe

126 reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also

127 n cardiomyocytes and partial protection from ischemia-reperfusion injury by reducing mitochondrial pe

128 helial Phd2 ablation protected against renal ischemia-reperfusion injury by suppressing the expressio

129 Hepatic ischemia-reperfusion injury can result in organ failure,

130 an prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart

131 variety of pathological disorders including ischemia/reperfusion injury, cataract formation, and neu

132 n in vehicle-treated db/db mice subjected to ischemia/reperfusion injury compared with control mice.

133 or of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phen

134 Cold ischemia and reversible ischemia-reperfusion injury dampened antigen presentatio

135 This system is especially important in ischemia-reperfusion injury/delayed graft function as we

136 recover renal function, possibly because of ischemia/reperfusion injury developing after PTRA.

137 ration and modifies the pathology in a renal ischemia/reperfusion-injury disease model, via its effec

138 ximately 50% 24 h after an in vitro model of ischemia/reperfusion injury, due to delayed fragmentatio

139 Ischemia-reperfusion injury during hepatic resection has

140 In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, ph

141 pathogenesis of inflammatory bowel disease, ischemia-reperfusion injury, enteroinvasive bacterial an

142 in mouse kidneys 18 months after a bilateral ischemia/reperfusion injury event.

143 cipients and patients, who are vulnerable to ischemia reperfusion injury following restoration of cor

144 The extent to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly stud

145 estigated in cerebral, myocardial, and renal ischemia reperfusion injury; helium and xenon have addit

146 results describe a role for Plexin C1 during ischemia-reperfusion injury, highlight the role of hemat

147 get of rapamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and steatot

148 (H2S) is an attractive agent for myocardial ischemia-reperfusion injury, however, systemic delivery

149 well recognized in the context of sepsis and ischemia-reperfusion injury; however, it also occurs in

150 Ischemia reperfusion injury (I/RI) is a common complicat

151 system and leading to recurrent episodes of ischemia-reperfusion injury (I/RI) to multiple organ sys

152 SPCs) on the cerebral microcirculation after ischemia-reperfusion injury (I/RI).

153 nticoagulant HS oligosaccharides limit liver ischemia reperfusion injury in a mouse model.

154 en attributed to organ protective effects in ischemia reperfusion injury in a variety of medical cond

155 izes metabolism to possibly better cope with ischemia reperfusion injury in discarded kidneys.

156 been shown to contribute to liver and kidney ischemia reperfusion injury in mice.

157 of donor renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congenei

158 ed to reverse protection from fibrosis after ischemia-reperfusion injury in ADAM17 hypomorphic mice;

159 ting its therapeutic potential in preventing ischemia-reperfusion injury in heart transplant.

160 ehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats.

161 y predict efficacy in vivo, DMX-5804 reduces ischemia-reperfusion injury in mice by more than 50%.

162 plays a pivotal role in the pathogenesis of ischemia-reperfusion injury in solid organ transplantati

163 d quantified and compared renal responses to ischemia-reperfusion injury in the presence and absence

164 We induced ischemia/reperfusion injury in livers of mice given a sm

165 rventions as a therapeutic approach to limit ischemia/reperfusion injury in mammals.

166 SEP and L-Cit on diabetic cardiomyopathy and ischemia/reperfusion injury in obese type 2 diabetic mic

167 ine kidney lysates, which is elevated during ischemia/reperfusion injury in vivo This induced nuclear

168 Ischemia-reperfusion injury induced influx of monocytes,

169 le of detecting both nephrotoxin-induced and ischemia-reperfusion injury-induced AKI in live mice.

170 Ischemia reperfusion injury induces a systemic increase

171 by early insults to the allograft, including ischemia/reperfusion injury, infections, and rejection.

172 ion molecule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased f

173 impaired oxygen supply to the periphery and ischemia reperfusion injury, inflammation, oxidative str

174 Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation

175 flow during organ procurement, and prolonged ischemia-reperfusion injury IRI results in increased rat

176 sm, but it also contributes significantly to ischemia reperfusion injury (IRI) associated with myocar

177 Ischemia reperfusion injury (IRI) during liver-metastasi

178 s were assessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in high-fat diet (HFD)

179 Ischemia reperfusion injury (IRI) predisposes to the for

180 formin in C57BL/6 mice challenged with renal ischemia reperfusion injury (IRI), treated before or aft

181 es to the high sensitivity of aged livers to ischemia reperfusion injury (IRI).

182 jured and repairing kidneys on day two after ischemia reperfusion injury (IRI).

183 aft survival and correlates with severity of ischemia reperfusion injury (IRI).

184 This phenomenon is called ischemia reperfusion injury (IRI).

185 on and cardiomyocyte injury are hallmarks of ischemia-reperfusion injury (IRI) after heart transplant

186 Complement plays important roles in both ischemia-reperfusion injury (IRI) and antibody-mediated

187 her/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes.

188 modulatory mechanism that protects mice from ischemia-reperfusion injury (IRI) and subsequent AKI.

189 Using rat renal ischemia-reperfusion injury (IRI) as a model of acute ki

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

191 les show an improved ability to recover from ischemia-reperfusion injury (IRI) compared with males; h

192 inal aortic aneurysm (AAA) repair results in ischemia-reperfusion injury (IRI) in local (i.e. kidney)

193 , and S1P5), and S1PR agonists reduce kidney ischemia-reperfusion injury (IRI) in mice.

194 t regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but t

195 ctors have been implicated in the process of ischemia-reperfusion injury (IRI) in organ transplantati

196 e of CD47 signaling has been shown to reduce ischemia-reperfusion injury (IRI) in various models of t

197 Ischemia-reperfusion injury (IRI) is a complex inflammat

198 Ischemia-reperfusion injury (IRI) is a leading cause of

199 Ischemia-reperfusion injury (IRI) is a major cause of AK

200 Ischemia-reperfusion injury (IRI) is an important cause

201 Ischemia-reperfusion injury (IRI) is an important risk f

202 rotection by activated protein C (aPC) after ischemia-reperfusion injury (IRI) is associated with apo

203 Ischemia-reperfusion injury (IRI) is believed to contrib

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

205 Ischemia-reperfusion injury (IRI) leading to delayed gra

206 Renal ischemia-reperfusion injury (IRI) leads to acute kidney

207 s in lymphoid organs and protected mice from ischemia-reperfusion injury (IRI) more efficiently than

208 e of the CD47 signaling pathway could reduce ischemia-reperfusion injury (IRI) of renal allografts do

209 Here, genes related to ischemia-reperfusion injury (IRI) or graft rejection may

210 Liver ischemia-reperfusion injury (IRI) represents a major ris

211 We studied proximal tubules after ischemia-reperfusion injury (IRI) to characterize possib

212 Substantial ischemia-reperfusion injury (IRI) to the transplanted ki

213 lammation is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic

214 The ischemia-reperfusion injury (IRI) was analyzed through h

215 y allow directed pharmacomodulation of renal ischemia-reperfusion injury (IRI) without the need for s

216 of tubular epithelial cell repair following ischemia-reperfusion injury (IRI), a common type of rena

217 , how this diverse population is affected by ischemia-reperfusion injury (IRI), an obligate part of r

218 s (DAMPs) released from cells damaged during ischemia-reperfusion injury (IRI), in heart attack or st

219 Following renal ischemia-reperfusion injury (IRI), resolution of inflamm

220 le genetic approach in a mouse model of AKI, ischemia-reperfusion injury (IRI), to determine the temp

221 ial liver uptake to directly prevent hepatic ischemia-reperfusion injury (IRI), which is a reactive o

222 Steatotic livers are more susceptible to ischemia-reperfusion injury (IRI), which is exacerbated

223 ulation of the vagus nerve attenuates kidney ischemia-reperfusion injury (IRI), which promotes the re

224 ific NF-kappaB signaling in a mouse model of ischemia-reperfusion injury (IRI)-induced AKI.

225 in expression, at 1 h after AKI triggered by ischemia-reperfusion injury (IRI).

226 C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI).

227 trategy for organ preservation which reduces ischemia-reperfusion injury (IRI).

228 , the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined.

229 Ischemia/reperfusion injury (IRI) following conventional

230 Here, using a murine renal ischemia/reperfusion injury (IRI) model, we show that in

231 Inflammatory responses associated with ischemia/reperfusion injury (IRI) play a central role in

232 After bilateral kidney ischemia/reperfusion injury (IRI), monocytes infiltrate

233 c steatosis renders liver more vulnerable to ischemia/reperfusion injury (IRI), which commonly occurs

234 espond via this pathway to imposed pulmonary ischemia/reperfusion injury (IRI).

235 Liver ischemia reperfusion injury is associated with coagulati

236 Hepatic ischemia-reperfusion injury is a disease pattern that is

237 Ischemia-reperfusion injury is inevitable during intesti

238 ndications that the inflammatory response to ischemia-reperfusion injury is mediated by cyclooxygenas

239 circulating proinflammatory cytokines during ischemia-reperfusion injury is not well understood.

240 Lung ischemia-reperfusion injury is the main cause of primary

241 Ischemia-reperfusion injury is unavoidably caused by los

242 Hepatic ischemia/reperfusion injury is a complication of liver s

243 e), in two mouse CKD models, UUO and chronic ischemia reperfusion injury, led to a reduction in fibro

244 At 33 days after ischemia/reperfusion injury, LNA-21-treated hearts exhib

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

246 Ischemia-reperfusion injury may compromise the short-ter

247 Myocardial ischemia-reperfusion injury (MIRI) is a serious threat t

248 nt of THP(-/-) mice with truncated THP after ischemia-reperfusion injury mitigated the worsening of A

249 Results of this study in a renal ischemia-reperfusion injury model allow phenotype and fu

250 ce lacking periostin expression in the renal ischemia-reperfusion injury model, and primary cultures

251 fect of amniotic fluid stem cells in a renal ischemia-reperfusion injury model.

252 owth factor secretion, and performance in an ischemia/reperfusion injury model.

253 an protective effects mostly in small animal ischemia reperfusion injury models.

254 protection in a model of heart damage termed ischemia-reperfusion injury, motivating further study of

255 phils in a human-disease-relevant myocardial ischemia reperfusion injury mouse model after i.v. injec

256 In this study, we used a renal bilateral ischemia-reperfusion injury mouse model to identify uniq

257 u- and (68)Ga-DOTA-ECL1i were compared in an ischemia-reperfusion injury mouse model.

258 ic brain or spinal cord injury, glaucoma and ischemia-reperfusion injury of the eye.

259 herosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex.

260 regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-deri

261 Hepatic ischemia-reperfusion injury or sham operation.

262 We subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstr

263 kout mice were protected from fibrosis after ischemia-reperfusion injury or unilateral ureteral obstr

264 t is highly upregulated with injury, we used ischemia-reperfusion injury or unilateral ureteral obstr

265 the donor pool, protect these livers against ischemia-reperfusion injury, or improve their quality be

266 In an ex vivo model of cardiac ischemia/reperfusion injury, perfusion of a mouse heart

267 After ischemia-reperfusion injury, periostin-overexpressing mi

268 plasma samples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to renal tra

269 is associated with various diseases such as ischemia/reperfusion injury, polycystic kidney disease,

270 doxically, it preserves heart function after ischemia/reperfusion injury, potentially by decreasing p

271 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effec

272 Similarly, in a rat model of renal ischemia/reperfusion injury, SAR247799 preserved renal s

273 inflammation within the muscle tissue during ischemia/reperfusion injury sensitizes group III and IV

274 In conclusion, in this rat model of ischemia-reperfusion injury, sigma1-receptor agonists im

275 cal conditions such as rheumatoid arthritis, ischemia/reperfusion injury, stroke, diabetic vasculopat

276 ng pathway can afford protection against the ischemia/reperfusion injury that occurs during myocardia

277 Because of its susceptibility to ischemia-reperfusion injury, the heart can be preserved

278 After ischemia-reperfusion injury, THP(-/-) mice, compared wit

279 Therapeutic trials aimed at prevention of ischemia/reperfusion injury to allografts based on anima

280 Mice were then subjected to cardiac ischemia/reperfusion injury to depress heart function, f

281 e to resolve tubular injury after unilateral ischemia-reperfusion injury (U-IRI) led to sustained low

282 Compared with controls, mouse models of ischemia-reperfusion injury, urinary obstruction, and hy

283 in a preclinical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion fo

284 tect the heart against subsequent myocardial ischemia/reperfusion injury via direct effects on the my

285 This reduction in ischemia-reperfusion injury was accompanied by reduced n

286 Mesenteric ischemia-reperfusion injury was induced in male Wistar r

287 Myocardial ischemia-reperfusion injury was induced via left anterio

288 Ischemia-reperfusion injury was modeled in vitro by plac

289 jury in kidneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the absen

290 ntravital microscopy, we found that cerebral ischemia/reperfusion injury was accompanied by neutrophi

291 , in vivo kidney fibrosis induced via UUO or ischemia/reperfusion injury was ameliorated by systemic

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

293 tor-amniotic fluid stem cells can worsen the ischemia-reperfusion injury when delivered in a high dos

294 coronary artery ligation-induced myocardial ischemia reperfusion injury where inhibition of ferropto

295 non have additionally been tested in hepatic ischemia reperfusion injury, whereas neon was only explo

296 iency of endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation of end

297 expression of proregenerative factors after ischemia-reperfusion injury, whereas knockout mice exhib

298 annels renders the heart more susceptible to ischemia/reperfusion injury, whereas the pathological ev

299 inal organs have a higher risk of developing ischemia-reperfusion injury, which can lead to posttrans

300 -)) protects against experimental myocardial ischemia/reperfusion injury with reduced infarct size an