ライフサイエンスコーパス: reperfusion injury

1 es such as chronic inflammation and ischemia-reperfusion injury.

2 phagy, mPTP opening, and death with ischemia/reperfusion injury.

3 rimental animal models of acute ischemia and reperfusion injury.

4 tive and inhibits cardiac allograft ischemia-reperfusion injury.

5 ient to decrease infarct size after ischemia/reperfusion injury.

6 having a shorter CIT due to severe ischemia reperfusion injury.

7 cious in an animal model of kidney ischaemia reperfusion injury.

8 oimmunity, and aggravates damage in ischemia/reperfusion injury.

9 lung function and resilience to ischemia and reperfusion injury.

10 asma attenuates age-dependent liver ischemia reperfusion injury.

11 rdial injection in a mouse model of ischemia reperfusion injury.

12 9 inhibition largely abolished warm ischemia-reperfusion injury.

13 cardiac physiology and response to ischemia/reperfusion injury.

14 /-) mice were challenged with renal ischemia-reperfusion injury.

15 endent thromboinflammation during myocardial reperfusion injury.

16 of this treatment in reducing early ischemia-reperfusion injury.

17 vates a cardioprotective program that limits reperfusion injury.

18 method to protect the heart against ischemia reperfusion injury.

19 hil has a role in murine intestinal ischemia/reperfusion injury.

20 presence of regulatory T cell after ischemia-reperfusion injury.

21 ent with necrostatin-1 during renal ischemia-reperfusion injury.

22 poptosis in epithelial cells during ischemia-reperfusion injury.

23 this compound as a novel adjunct therapy for reperfusion injury.

24 and delivered to athymic rats after ischemia-reperfusion injury.

25 vity is required to protect against ischemia/reperfusion injury.

26 ed by folic acid (FA) or unilateral ischemia-reperfusion injury.

27 emia/reperfusion reduces myocardial ischemia/reperfusion injury.

28 sensitizes the heart to myocardial ischemia/reperfusion injury.

29 -derived exosomes in a rat model of ischemia-reperfusion injury.

30 times and to ameliorate the consequences of reperfusion injury.

31 ) model was used to establish brain ischemia-reperfusion injury.

32 tory response after sublethal renal ischemia-reperfusion injury.

33 al deficits than sTM after cerebral ischemia/reperfusion injury.

34 models of systemic inflammation and ischemia-reperfusion injury.

35 1 neurons: protection against renal ischemia-reperfusion injury.

36 cultures using an in vitro model of ischemia reperfusion injury.

37 tromechanical uncoupling, and acute ischemia/reperfusion injury.

38 le inflammation that follows kidney ischemia-reperfusion injury.

39 intensely loud noise exposures and ischemia-reperfusion injury.

40 ffects in models of endotoxemia and ischemia-reperfusion injury.

41 novel contributor and therapeutic target of reperfusion injury.

42 in directly activated by cAMP 1) in ischemia/reperfusion injury.

43 rit but also a victim of myocardial ischemia/reperfusion injury.

44 ted in a rodent model of myocardial ischemia-reperfusion injury.

45 rtuin 1 is protective after hepatic ischemia-reperfusion injury.

46 significant role in mouse models of ischemia-reperfusion injury.

47 ophysiological processes including ischaemia-reperfusion injury.

48 els suggest that C1-INH ameliorates ischemia-reperfusion injury.

49 aminophen hepatotoxicity or hepatic ischemia-reperfusion injury.

50 isms involved in the development of ischemia-reperfusion injury.

51 -mediated protection against kidney ischemia/reperfusion injury.

52 eon was only explored in myocardial ischemia reperfusion injury.

53 nscriptional changes observed after ischemia-reperfusion injury.

54 ective effects in patients with ischemia and reperfusion injury.

55 nflammatory pathways after cerebral ischemia/reperfusion injury.

56 al rejuvenation to the heart after ischaemia-reperfusion injury.

57 orted to have a detrimental role in ischemia-reperfusion injury.

58 mRNA and protein are induced after ischemia-reperfusion injury.

59 tory properties that could minimize ischemia reperfusion injury.

60 utic potential in diseases, such as ischemic reperfusion injury.

61 ne defense and highly vulnerable to ischemia-reperfusion injury.

62 myoblasts from an in vitro model of ischemic reperfusion injury.

63 nd improved tissue repair following ischemia-reperfusion injury.

64 n of PHD2 in a mouse model of renal ischemia-reperfusion injury.

65 al fibrosis 28 days post-myocardial ischemia-reperfusion injury.

66 of mitochondrial recovery following ischemia-reperfusion injury.

67 ning in mice before and after renal ischemia-reperfusion injury.

68 reasing liver damage resulting from ischemia reperfusion injury.

69 troke infarct volume after cerebral ischemia-reperfusion injury.

70 eutrophil extravasation and ischemia-induced reperfusion injury.

71 ay better protect these organs from ischemia-reperfusion injury.

72 tophagy is important for mitigating ischemia/reperfusion injury.

73 odels and livers of mice undergoing ischemia/reperfusion injury.

74 asound scan, against prolonged cold ischemia-reperfusion injury (24 hours at 4 degrees C), along with

75 tive effect of these noble gases on ischemia reperfusion injury across a broad range of experimental

76 developed to protect patients from ischemia/reperfusion injury after liver surgery or for other hepa

77 s, including myocardial infarction, ischemia-reperfusion injury after myocardial infarction, and hear

78 ing reactive oxygen species (ROS) underlying reperfusion injury after prolonged cardiac ischemia.

79 Lung ischemia-reperfusion injury after transplantation is associated w

80 ic inflammatory diseases, including ischemia/reperfusion injury, allergic asthma, autoimmune nephriti

81 protected the liver against lethal ischemia/reperfusion injury, allowing 100% survival rate.

82 Ischemia-reperfusion injury also promoted DC-dependent cross-pres

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

84 ns in vascular inflammation such as ischemia-reperfusion injury and cardiovascular diseases.

85 rly phase of kidney transplant when ischemia-reperfusion injury and cyclosporin A toxicity may coexis

86 e as pathogenically contributing to ischemia-reperfusion injury and delayed graft function (DGF) in h

87 argon was only possible in cerebral ischemia reperfusion injury and did not show neuroprotective effe

88 ic cardiac transplantation to model ischemia-reperfusion injury and distinguish tissue-resident from

89 lineated as a genuine factor contributing to reperfusion injury and graft dysfunction after transplan

90 a/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' prognosis after

91 ose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function, demonst

92 B destruction attenuates myocardial ischemia-reperfusion injury and may avoid unwanted side effects.

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

94 f exercise on metabolic parameters, ischemia-reperfusion injury and regeneration after hepatectomy.

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

96 nct donor macrophage populations in ischemia-reperfusion injury and rejection, including their intera

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

98 ological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and neurolog

99 e a better understanding of cardiac ischemia-reperfusion injury and the various possibilities to limi

100 tory tissue damage in, for example, ischemia-reperfusion injury and transplant rejection yet is benef

101 The patients in the low-PF group had severe reperfusion injury and were more frequently complicated

102 e subjected to ex vivo reperfusion, modeling reperfusion injury and were similarly analyzed for energ

103 toneal contamination and infection, ischemia-reperfusion-injury and glycerol-induced acute kidney-inj

104 'deactive transition' (relevant to ischemia-reperfusion injury) and their effects on the ubiquinone-

105 uromuscular diseases of childhood, ischaemia-reperfusion injury, and age-related neurodegenerative di

106 f-1 bound prohibitin-2 during renal ischemia/reperfusion injury, and Bif-1-deficiency protected again

107 an array of human diseases including asthma, reperfusion injury, and cancer.

108 sis for cell therapy in mice after ischaemia-reperfusion injury, and find that-although heart functio

109 on field, has shown to reduce liver ischemia-reperfusion injury, and has shown to decrease the graft

110 diomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac function in isc

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

112 obesity and type 2 diabetes (T2D), ischemia-reperfusion injury, and neurodegenerative diseases.

113 rmal kidney and following bilateral ischemia-reperfusion injury, and quantified and compared renal re

114 ity improved cardiac recovery after ischemia/reperfusion injury, and the response was similar with be

115 The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, f

116 maphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the levels of lactate

117 /Nrf2 signaling in mice with UUO or ischemia/reperfusion injury, as well as in cultured human kidney

118 on overload protected against renal ischemia-reperfusion injury-associated sterile inflammation.

119 ted within a few hours of bilateral ischemia-reperfusion injury at these sites and new sites of proxi

120 ximal tubule deletion of DRP1 after ischemia-reperfusion injury attenuated progressive kidney injury

121 Administration of C31 in mice with ischemia/reperfusion injury before and during reperfusion restore

122 the patients in the high-PF group had milder reperfusion injury, but had lower intraoperative hepatic

123 ture and cardiomyocyte death during ischemia-reperfusion injury by inducing mitochondrial permeabilit

124 ents age-related intolerance to ischemia and reperfusion injury by modulating substrate metabolism.

125 an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also provides

126 yocytes and partial protection from ischemia-reperfusion injury by reducing mitochondrial permeabilit

127 d2 ablation protected against renal ischemia-reperfusion injury by suppressing the expression of proi

128 Here, we demonstrate that metoprolol reduces reperfusion injury by targeting the haematopoietic compa

129 t death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage.

130 Hepatic ischemia-reperfusion injury can result in organ failure, which is

131 d the effect of LV unloading on ischemia and reperfusion injury, cardiac metabolism, and mitochondria

132 of pathological disorders including ischemia/reperfusion injury, cataract formation, and neurodegener

133 cle-treated db/db mice subjected to ischemia/reperfusion injury compared with control mice.

134 or renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and

135 Cold ischemia and reversible ischemia-reperfusion injury dampened antigen presentation by rena

136 s system is especially important in ischemia-reperfusion injury/delayed graft function as well as in

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

138 d modifies the pathology in a renal ischemia/reperfusion-injury disease model, via its effects on Wnt

139 50% 24 h after an in vitro model of ischemia/reperfusion injury, due to delayed fragmentation and mit

140 Ischemia-reperfusion injury during hepatic resection has been sho

141 In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes

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

143 and patients, who are vulnerable to ischemia reperfusion injury following restoration of coronary blo

144 nt to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly studied.

145 in cerebral, myocardial, and renal ischemia reperfusion injury; helium and xenon have additionally b

146 pamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and steatotic liver

147 an attractive agent for myocardial ischemia-reperfusion injury, however, systemic delivery of H2S ma

148 gnized in the context of sepsis and ischemia-reperfusion injury; however, it also occurs in organ tra

149 ary experimental approach, that ischemia and reperfusion injury (I/R) in male Swiss Webster mice alte

150 Ischemia reperfusion injury (I/RI) is a common complication of ca

151 nd leading to recurrent episodes of ischemia-reperfusion injury (I/RI) to multiple organ systems.

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

153 een extensively used to investigate ischemic-reperfusion injury, immunological consequences during he

154 renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congeneic renal t

155 ant HS oligosaccharides limit liver ischemia reperfusion injury in a mouse model.

156 erse protection from fibrosis after ischemia-reperfusion injury in ADAM17 hypomorphic mice; injected

157 bolism to possibly better cope with ischemia reperfusion injury in discarded kidneys.

158 therapeutic potential in preventing ischemia-reperfusion injury in heart transplant.

159 We induced ischemia/reperfusion injury in livers of mice given a small-molec

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

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

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

163 pivotal role in the pathogenesis of ischemia-reperfusion injury in solid organ transplantation.

164 mirococept (APT070) for preventing ischaemia-reperfusion injury in the kidney allograft (EMPIRIKAL) t

165 ied and compared renal responses to ischemia-reperfusion injury in the presence and absence of GDF15.

166 nd on ferroptosis-associated renal ischaemia-reperfusion injury in vivo.

167 the pathophysiology of myocardial ischaemia-reperfusion injury, including the role of autophagy and

168 otective effects against myocardial ischemic/reperfusion injury, indicating their potential applicati

169 Ischemia-reperfusion injury induced influx of monocytes, DCs, mac

170 ecting both nephrotoxin-induced and ischemia-reperfusion injury-induced AKI in live mice.

171 Ischemia reperfusion injury induces a systemic increase of cf-mt-

172 insults to the allograft, including ischemia/reperfusion injury, infections, and rejection.

173 ule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased function i

174 oxygen supply to the periphery and ischemia reperfusion injury, inflammation, oxidative stress, and

175 Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation is mediat

176 ng organ procurement, and prolonged ischemia-reperfusion injury IRI results in increased rates of del

177 ement plays important roles in both ischemia-reperfusion injury (IRI) and antibody-mediated rejection

178 EACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes.

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

180 hogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined.

181 Using rat renal ischemia-reperfusion injury (IRI) as a model of acute kidney inju

182 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with increased expre

183 t also contributes significantly to ischemia reperfusion injury (IRI) associated with myocardial infa

184 Ischemia reperfusion injury (IRI) during liver-metastasis resecti

185 Ischemia/reperfusion injury (IRI) following conventional cold sto

186 sessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in high-fat diet (HFD)-fed mice

187 ic aneurysm (AAA) repair results in ischemia-reperfusion injury (IRI) in local (i.e. kidney) and dist

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

189 ors CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but the effect

190 signaling has been shown to reduce ischemia-reperfusion injury (IRI) in various models of tissue isc

191 Ischemia-reperfusion injury (IRI) is a complex inflammatory proce

192 Ischemia-reperfusion injury (IRI) is a leading cause of AKI.

193 Ischemia-reperfusion injury (IRI) is an important cause of acute

194 Ischemia-reperfusion injury (IRI) is an important risk factor for

195 Ischemia and reperfusion injury (IRI) is an inevitable event in conve

196 by activated protein C (aPC) after ischemia-reperfusion injury (IRI) is associated with apoptosis in

197 Ischemia-reperfusion injury (IRI) is believed to contribute to gr

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

199 Ischemia-reperfusion injury (IRI) leading to delayed graft functi

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

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

202 hoid organs and protected mice from ischemia-reperfusion injury (IRI) more efficiently than either cy

203 CD47 signaling pathway could reduce ischemia-reperfusion injury (IRI) of renal allografts donated aft

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

205 lammatory responses associated with ischemia/reperfusion injury (IRI) play a central role in alloimmu

206 Ischemia reperfusion injury (IRI) predisposes to the formation of

207 Liver ischemia and reperfusion injury (IRI) remains a serious clinical prob

208 Liver ischemia-reperfusion injury (IRI) represents a major risk factor

209 is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic events,

210 The ischemia-reperfusion injury (IRI) was analyzed through histologic

211 irected pharmacomodulation of renal ischemia-reperfusion injury (IRI) without the need for systemic d

212 ar epithelial cell repair following ischemia-reperfusion injury (IRI), a common type of renal stresso

213 s diverse population is affected by ischemia-reperfusion injury (IRI), an obligate part of renal tran

214 those seen in autoimmune diseases, ischemic reperfusion injury (IRI), and tissue transplant rejectio

215 released from cells damaged during ischemia-reperfusion injury (IRI), in heart attack or stroke sett

216 After bilateral kidney ischemia/reperfusion injury (IRI), monocytes infiltrate the kidne

217 Following renal ischemia-reperfusion injury (IRI), resolution of inflammation all

218 C57BL/6 mice challenged with renal ischemia reperfusion injury (IRI), treated before or after injury

219 is renders liver more vulnerable to ischemia/reperfusion injury (IRI), which commonly occurs in trans

220 uptake to directly prevent hepatic ischemia-reperfusion injury (IRI), which is a reactive oxygen spe

221 appaB signaling in a mouse model of ischemia-reperfusion injury (IRI)-induced AKI.

222 sion, at 1 h after AKI triggered by ischemia-reperfusion injury (IRI).

223 high sensitivity of aged livers to ischemia reperfusion injury (IRI).

224 a this pathway to imposed pulmonary ischemia/reperfusion injury (IRI).

225 lation (10 min) protected mice from ischemia-reperfusion injury (IRI).

226 repairing kidneys on day two after ischemia reperfusion injury (IRI).

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

228 or organ preservation which reduces ischemia-reperfusion injury (IRI).

229 recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardiomyocytes are a known

230 Hepatic ischemia/reperfusion injury is a complication of liver surgery th

231 Liver ischemia reperfusion injury is associated with coagulation and in

232 und After acute myocardial infarction (AMI), reperfusion injury is associated with microvascular lesi

233 Ischemia-reperfusion injury is inevitable during intestinal trans

234 Reperfusion injury is largely attributed to excess mitoc

235 ng proinflammatory cytokines during ischemia-reperfusion injury is not well understood.

236 A feasible therapy targeting reperfusion injury is remote ischemic conditioning (RIC)

237 Ischemia-reperfusion injury is unavoidably caused by loss and sub

238 At 33 days after ischemia/reperfusion injury, LNA-21-treated hearts exhibited redu

239 fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic, angiogenic, and

240 is key to improving outcomes, yet consequent reperfusion injury may be harmful.

241 Ischemia-reperfusion injury may compromise the short-term and lon

242 Myocardial ischemia-reperfusion injury (MIRI) is a serious threat to the hea

243 (-/-) mice with truncated THP after ischemia-reperfusion injury mitigated the worsening of AKI.

244 g periostin expression in the renal ischemia-reperfusion injury model, and primary cultures of isolat

245 mniotic fluid stem cells in a renal ischemia-reperfusion injury model.

246 or secretion, and performance in an ischemia/reperfusion injury model.

247 tive effects mostly in small animal ischemia reperfusion injury models.

248 a human-disease-relevant myocardial ischemia reperfusion injury mouse model after i.v. injection conf

249 is study, we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocy

250 8)Ga-DOTA-ECL1i were compared in an ischemia-reperfusion injury mouse model.

251 ic vascular complications, cardiac ischaemia-reperfusion injury, myocardial infarction, heart failure

252 osis and affords protection against ischemia/reperfusion injury of the cerebral cortex.

253 or spinal cord injury, glaucoma and ischemia-reperfusion injury of the eye.

254 ge of AMI/R and necrosis in conjunction with reperfusion injury of the heart.

255 Severe ischaemia-reperfusion injury of the right kidney, with subsequent

256 g the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resid

257 were protected from fibrosis after ischemia-reperfusion injury or unilateral ureteral obstruction de

258 ly upregulated with injury, we used ischemia-reperfusion injury or unilateral ureteral obstruction in

259 subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstruction.

260 pool, protect these livers against ischemia-reperfusion injury, or improve their quality before impl

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

262 After ischemia-reperfusion injury, periostin-overexpressing mice exhibi

263 amples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to renal transplantat

264 Post-ischemic reperfusion injury (PIRI) triggers an intense inflammato

265 se after brain death (BD) and posttransplant reperfusion injury play significant roles in the pathoge

266 ry blood flow after a heart attack can cause reperfusion injury potentially leading to impaired cardi

267 , it preserves heart function after ischemia/reperfusion injury, potentially by decreasing proteolysi

268 that promotes recovery from anoxia, reduces reperfusion injury, prevents oedema, and metabolically s

269 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effective ther

270 se lungs exhibited baseline induction of the reperfusion injury salvage kinase pathway but were less

271 Similarly, in a rat model of renal ischemia/reperfusion injury, SAR247799 preserved renal structure

272 In conclusion, in this rat model of ischemia-reperfusion injury, sigma1-receptor agonists improved po

273 tions such as rheumatoid arthritis, ischemia/reperfusion injury, stroke, diabetic vasculopathy, epile

274 y can afford protection against the ischemia/reperfusion injury that occurs during myocardial infarct

275 Because of its susceptibility to ischemia-reperfusion injury, the heart can be preserved for only

276 After ischemia-reperfusion injury, THP(-/-) mice, compared with wild-ty

277 eutic trials aimed at prevention of ischemia/reperfusion injury to allografts based on animal data sh

278 Mice were then subjected to cardiac ischemia/reperfusion injury to depress heart function, followed b

279 Because of the potential ischaemia-reperfusion injury to the kidney, we hypothesized that i

280 lve tubular injury after unilateral ischemia-reperfusion injury (U-IRI) led to sustained low-level Ch

281 ared with controls, mouse models of ischemia-reperfusion injury, urinary obstruction, and hypertensio

282 linical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion for 60 minu

283 tan protects against myocardial ischemia and reperfusion injury via vascular integrity preservation.

284 This reduction in ischemia-reperfusion injury was accompanied by reduced numbers of

285 kidney fibrosis induced via UUO or ischemia/reperfusion injury was ameliorated by systemic genetic k

286 Mesenteric ischemia-reperfusion injury was induced in male Wistar rats (six

287 Myocardial ischemia-reperfusion injury was induced via left anterior descend

288 Ischemia-reperfusion injury was modeled in vitro by placing human

289 idneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the absence of cla

290 ng a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against

291 en the central importance of mitochondria in reperfusion injury, we hypothesized that compared with i

292 tic fluid stem cells can worsen the ischemia-reperfusion injury when delivered in a high dose.

293 artery ligation-induced myocardial ischemia reperfusion injury where inhibition of ferroptosis resul

294 endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation of endothelial

295 on of proregenerative factors after ischemia-reperfusion injury, whereas knockout mice exhibited the

296 additionally been tested in hepatic ischemia reperfusion injury, whereas neon was only explored in my

297 nders the heart more susceptible to ischemia/reperfusion injury, whereas the pathological events elic

298 ns have a higher risk of developing ischemia-reperfusion injury, which can lead to posttransplant com

299 were analyzed in mouse models of myocardial reperfusion injury with genetic and pharmacological depl

300 cts against experimental myocardial ischemia/reperfusion injury with reduced infarct size and cardiom