ライフサイエンスコーパス: reperfusion injury

1 schemia and subsequent reperfusion (ischemia/reperfusion injury).

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

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

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

5 ophysiological processes including ischaemia-reperfusion injury.

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

7 aminophen hepatotoxicity or hepatic ischemia-reperfusion injury.

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

9 -mediated protection against kidney ischemia/reperfusion injury.

10 eon was only explored in myocardial ischemia reperfusion injury.

11 ective effects in patients with ischemia and reperfusion injury.

12 nflammatory pathways after cerebral ischemia/reperfusion injury.

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

14 perior renal function 30 days after ischemia/reperfusion injury.

15 hondrial reactive oxygen species in ischemia/reperfusion injury.

16 protective functions after cerebral ischemia/reperfusion injury.

17 recipient rat hearts 1 month after ischemia reperfusion injury.

18 c strategy in mitigating myocardial ischemia-reperfusion injury.

19 (FX06) has been proven to attenuate ischemia/reperfusion injury.

20 The pathogenesis of PGD involves ischemia-reperfusion injury.

21 nd there were too few data on renal ischemia reperfusion injury.

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

23 1 in a mouse model of early hepatic ischemia-reperfusion injury.

24 restricted by cold preservation and ischemia-reperfusion injury.

25 eral nephrectomy plus contralateral ischemia-reperfusion injury.

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

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

28 ary occlusion inevitably results in ischemia-reperfusion injury.

29 also demonstrated decreased hepatic ischemia-reperfusion injury.

30 nterfering RNA is effective against ischemia-reperfusion injury.

31 for reducing the extent of hepatic ischemia-reperfusion injury.

32 athological mechanism in myocardial ischemia/reperfusion injury.

33 haride (LPS) pretreatment on kidney ischemia/reperfusion injury.

34 degrades heme and protects against ischemia-reperfusion injury.

35 the cerebral microcirculation after ischemia/reperfusion injury.

36 d activation of integrins for renal ischemia-reperfusion injury.

37 model, we delivered exosomes after ischemia-reperfusion injury.

38 alvage, larger infarcts, and more pronounced reperfusion injury.

39 and provide protection against ischemia and reperfusion injury.

40 The C1-INH treatment may reduce ischemia-reperfusion injury.

41 ote tissues and organs resistant to ischemia/reperfusion injury.

42 nd tissue selenium levels after ischemia and reperfusion injury.

43 er switch for various damage pathways during reperfusion injury.

44 ses in the early and late phases of ischemia-reperfusion injury.

45 ent, and future therapies to reduce ischemia/reperfusion injury.

46 protection on heart tissue against ischemia-reperfusion injury.

47 e that CD4(+) T-cells contribute to ischemia-reperfusion injury.

48 elenium distribution is affected by ischemia reperfusion injury.

49 ive in all tested models of cardiac ischemia-reperfusion injury.

50 nd less inflammatory response after ischemia/reperfusion injury.

51 nium would affect outcome after ischemia and reperfusion injury.

52 ells and contribute to acute kidney ischemia-reperfusion injury.

53 A (CsA) might protect the kidney from lethal reperfusion injury.

54 alleviated their susceptibility to ischemia/reperfusion injury.

55 nticipated therapeutic responses to ischemia-reperfusion injury.

56 tribute to the pathology of hepatic ischemia/reperfusion injury.

57 icated in the pathogenesis of renal ischemia-reperfusion injury.

58 n species (ROS) as a consequence of ischemia-reperfusion injury.

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

60 ptor (A2AR) agonism attenuates lung ischemia-reperfusion injury.

61 duction and protection from hepatic ischemia reperfusion injury.

62 l models of cerebral and myocardial ischemia/reperfusion injury.

63 cascade of events that is also harmful, viz. reperfusion injury.

64 st left anterior descending artery occlusion/reperfusion injury.

65 cause of tissue damage during renal ischemia-reperfusion injury.

66 ion and protects mice against renal ischemia-reperfusion injury.

67 oid cells were protected from renal ischemia-reperfusion injury.

68 cells and contributes to myocardial ischemia/reperfusion injury.

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

70 emia/reperfusion reduces myocardial ischemia/reperfusion injury.

71 sensitizes the heart to myocardial ischemia/reperfusion injury.

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

73 times and to ameliorate the consequences of reperfusion injury.

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

75 tory response after sublethal renal ischemia-reperfusion injury.

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

77 models of systemic inflammation and ischemia-reperfusion injury.

78 1 neurons: protection against renal ischemia-reperfusion injury.

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

80 tromechanical uncoupling, and acute ischemia/reperfusion injury.

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

82 le inflammation that follows kidney ischemia-reperfusion injury.

83 intensely loud noise exposures and ischemia-reperfusion injury.

84 poptosis in epithelial cells during ischemia-reperfusion injury.

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

86 novel contributor and therapeutic target of reperfusion injury.

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

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

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

90 The activity of COX contributes to ischemia-reperfusion injury after intestinal transplantation.

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

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

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

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

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

96 strategy proposed to prevent renal ischemia-reperfusion injuries and delayed graft function (DGF).

97 ed about mechanisms of neuronal ischemic and reperfusion injury and associated inflammation.

98 e destruction attenuates myocardial ischemia-reperfusion injury and could avoid unwanted side effects

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

100 role in the early phase of hepatic ischemia-reperfusion injury and determine the extent of tissue da

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

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

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

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

105 ctions but also plays a key role in ischemia-reperfusion injury and other inflammatory disorders.

106 Tissue necrosis as a consequence of ischemia-reperfusion injury and oxidative damage is a leading cau

107 suppression of miR-206 exacerbated ischemia/reperfusion injury and prevented pressure overload-induc

108 nce suggests that cyclosporine may attenuate reperfusion injury and reduce myocardial infarct size.

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

110 after AKI in two models: bilateral ischemia-reperfusion injury and unilateral nephrectomy plus contr

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

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

113 been implicated in the pathology of asthma, reperfusion injury, and cancer.

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

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

116 selenium levels decrease after ischemia and reperfusion injury, and low blood selenium correlates wi

117 d/or diagnosis of diabetes, cancer, ischemia/reperfusion injury, and neurodegenerative diseases.

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

119 ve emerged regarding mechanisms of ischaemia-reperfusion injury, and some hold promise as targets of

120 in C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Plexin C1 is a pote

121 and cNK cells and protected against ischemic/reperfusion injury, anti-AsGM1 Ab preferentially deplete

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

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

124 ation of normal metabolism and prevention of reperfusion injury, as this holds the promise of restori

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

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

127 table for transplantation due to the risk of reperfusion injury, but could be reconditioned using ex-

128 come to focus efforts on therapies to reduce reperfusion injury, but in the recent few years, few int

129 left ventricular function following ischemia/reperfusion injury, but its role in cardiac arrest is un

130 agonist, FTY720, attenuates kidney ischemia-reperfusion injury by directly activating S1P1 on proxim

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

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

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

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

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

136 eral diseases, including tissue ischemia and reperfusion injuries, cardiac hypertrophy and failure, a

137 iseases, including atherosclerosis, ischemia-reperfusion injury, cardiomyopathy, and heart failure.

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

139 Renal ischemia and reperfusion injury causes loss of renal epithelial cell

140 79 can protect mice against hepatic ischemia/reperfusion injury, chemical toxicity, and sepsis.

141 nificant added beneficial effect on ischemia-reperfusion injury compared to propofol.

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

143 strated increased susceptibility to ischemia-reperfusion injury compared with wild-type mice.

144 also leads to irreversible events including reperfusion injury, decreased cardiac function and ultim

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

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

147 50% 24 h after an in vitro model of ischemia/reperfusion injury, due to delayed fragmentation and mit

148 Ischemia-reperfusion injury during hepatic resection has been sho

149 etics such as sevoflurane attenuate ischemia-reperfusion injury during liver resection.

150 er from glycocalyx alterations, and ischemia-reperfusion injury during OLT further exacerbates its da

151 One month after ischemia/reperfusion injury, EHMs were implanted onto immunocompr

152 esis of inflammatory bowel disease, ischemia-reperfusion injury, enteroinvasive bacterial and parasit

153 he coronary artery in vivo protected against reperfusion injury, even in the presence of normal level

154 Three months after ischemia/reperfusion injury, Gottingen swine received transendoca

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

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

157 escribe a role for Plexin C1 during ischemia-reperfusion injury, highlight the role of hematopoietic

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

159 role of epigenetic modifications in ischemia-reperfusion injury, host immune response to the graft, a

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

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

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

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

164 he damage caused by brain death and ischemia-reperfusion injury in a rat model of kidney and heart tr

165 uted to organ protective effects in ischemia reperfusion injury in a variety of medical conditions, i

166 l interfering RNA could reduce lung ischemia-reperfusion injury in an ex vivo model reproducing the p

167 Therapeutic hypothermia (TH) attenuates reperfusion injury in comatose survivors of cardiac arre

168 limits diabetic cardiomyopathy and ischemia/reperfusion injury in db/db mice through a tetrahydrobio

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

170 n to contribute to liver and kidney ischemia reperfusion injury in mice.

171 -Cit on diabetic cardiomyopathy and ischemia/reperfusion injury in obese type 2 diabetic mice.

172 eported to reduce biomarkers of ischemic and reperfusion injury in patients undergoing cardiac surger

173 such as multiple sclerosis and for ischemia-reperfusion injury in the brain and heart.

174 bioavailability, and ameliorated myocardial reperfusion injury in the setting of severe hypertension

175 y lysates, which is elevated during ischemia/reperfusion injury in vivo This induced nuclear localiza

176 is critical for the development of ischemia/reperfusion injury in vivo.

177 I (left anterior descending artery occlusion/reperfusion injury) in wild-type and Sh2b3 knockout rats

178 Macrophages (Mo) are integral in ischemia/reperfusion injury-incited (I/R-incited) acute kidney in

179 Key processes of reperfusion injury include the formation of reactive oxy

180 Renal ischemia-reperfusion injury induced hepatosplenic iron export thr

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

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

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

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

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

186 rdiomyocyte injury are hallmarks of ischemia-reperfusion injury (IRI) after heart transplantation.

187 s a known risk factor for increased ischemia-reperfusion injury (IRI) and poor outcomes after liver t

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

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

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

191 rie and protein restriction against ischemia/reperfusion injury (IRI) but also implicate H2S in longe

192 an improved ability to recover from ischemia-reperfusion injury (IRI) compared with males; however, t

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

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

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

196 e been implicated in the process of ischemia-reperfusion injury (IRI) in organ transplantation.

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

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

199 Ischemia-reperfusion injury (IRI) is a major cause of AKI, and pr

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

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

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

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

204 Ischemia reperfusion injury (IRI) is one of the major causes of A

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

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

207 ultrasound regimen prevents kidney ischemia-reperfusion injury (IRI) likely via the splenic choliner

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

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

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

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

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

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

214 Ischemia-reperfusion injury (IRI), an innate immunity-driven loca

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

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

217 c approach in a mouse model of AKI, ischemia-reperfusion injury (IRI), to determine the temporal effe

218 date the role of DAP12 in pulmonary ischemia/reperfusion injury (IRI), we took advantage of a clinica

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

220 otic livers are more susceptible to ischemia-reperfusion injury (IRI), which is exacerbated by the th

221 f the vagus nerve attenuates kidney ischemia-reperfusion injury (IRI), which promotes the release of

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

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

224 val and correlates with severity of ischemia reperfusion injury (IRI).

225 hese mice and wild type controls to ischemia/reperfusion injury (IRI).

226 system significantly contributes to ischemia/reperfusion injury (IRI).

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

228 Hepatic ischemia-reperfusion injury is a disease pattern that is associat

229 Reperfusion injury is largely attributed to excess mitoc

230 Renal ischemia-reperfusion injury is mediated by a complex cascade of e

231 s that the inflammatory response to ischemia-reperfusion injury is mediated by cyclooxygenases and th

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

233 The etiology of retinal ischemia-reperfusion injury is orchestrated by complex and still

234 Lung ischemia-reperfusion injury is the main cause of primary graft dy

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

236 o mouse CKD models, UUO and chronic ischemia reperfusion injury, led to a reduction in fibrosis.

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

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

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

240 Results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to

241 In a transient cerebral ischemia/reperfusion injury model, Apoe(-/-) mice expressing fibr

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

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

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

245 n in a model of heart damage termed ischemia-reperfusion injury, motivating further study of eNOS deg

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

247 phic lateral sclerosis, sepsis, ischemic and reperfusion injury of heart, kidney and liver, pulmonary

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

249 le improving cardiac function after ischemia/reperfusion injury of the heart.

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

251 to investigate the effect of renal ischemia-reperfusion injury on systemic iron homeostasis and dete

252 as microRNA sponges and to control ischemia-reperfusion injury or act as epigenetic regulators.

253 Hepatic ischemia-reperfusion injury or sham operation.

254 de targets to reperfusing tissue and reduces reperfusion injury perhaps by affecting oxygen metabolis

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

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

257 iated with various diseases such as ischemia/reperfusion injury, polycystic kidney disease, and conge

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

259 serum creatinine in rats with renal ischemia-reperfusion injury, providing evidence for its therapeut

260 In cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) genera

261 expression, which is protective in ischemia-reperfusion injury, regulates trafficking of myeloid-der

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

263 w-potassium dextran (LPD) solution, ischemia-reperfusion injury remains a major contributor to early

264 In mouse hearts, ischemia/reperfusion injury resulted in acute JP2 down-regulation

265 Ischemia-reperfusion injury resulted in significantly worse renal

266 In summary, renal ischemia-reperfusion injury results in profound alterations in sy

267 cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 from both platelet

268 imal models of peritonitis, hepatic ischemia-reperfusion injury, Salmonella infection, uveitis and Sj

269 , extracellular signal-regulated kinase 1/2 (reperfusion injury salvage kinase [RISK] pathway), and s

270 mod-induced cardioprotection was mediated by reperfusion injury salvage kinase and survivor activatin

271 during acute MI reduced infarct size via the reperfusion injury salvage kinase and survivor activatin

272 mod treatment activated the cardioprotective reperfusion injury salvage kinase and survivor activatin

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

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

275 tion to mediate protection in renal ischemia-reperfusion injury, suggesting that hepcidin-ferroportin

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

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

278 protective mechanism against renal ischemia-reperfusion injury through inhibition of Galpha12.

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

280 ficant clinical protection against ischaemia-reperfusion injury, Type II diabetes and ageing.

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

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

283 so measured damage after myocardial ischemia reperfusion injury using morphometry, neutrophil accumul

284 heart against subsequent myocardial ischemia/reperfusion injury via direct effects on the myocardium.

285 microscopy, we found that cerebral ischemia/reperfusion injury was accompanied by neutrophil and pla

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

287 Ischemia-reperfusion injury was induced in lungs isolated from mi

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

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 elenium administration could reduce ischemia reperfusion injury, we synthesized and administered sodi

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

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

294 trophy and protected the heart from ischemia/reperfusion injury, whereas suppression of miR-206 exace

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

296 fl)/PF4-Cre mice showed dramatically reduced reperfusion injury which correlated with diminished form

297 ole of fibrin derivatives in global ischemia/reperfusion injury, which can be attenuated by the fibri

298 herapies are limited by the complications of reperfusion injury, which include increased cerebrovascu

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

300 ith innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeling after