ライフサイエンスコーパス: cardiac injury

1 ndicator of neuromuscular skeletal muscle or cardiac injury).

2 educe reactive oxygen species (ROS) -induced cardiac injury.

3 al-cell-like phenotype after acute ischaemic cardiac injury.

4 egenerative and nonregenerative responses to cardiac injury.

5 d a potential therapeutic target in ischemic cardiac injury.

6 y counteract substantial cell loss caused by cardiac injury.

7 itical mechanism in the maternal response to cardiac injury.

8 h an increase in this contribution following cardiac injury.

9 yte Ca(2)(+) homeostasis and survival during cardiac injury.

10 ac function and ventricular dilatation after cardiac injury.

11 rving cardiac function after acute ischaemic cardiac injury.

12 te immunity and ischemia/reperfusion-induced cardiac injury.

13 the biomarker of choice for the diagnosis of cardiac injury.

14 have potential as therapeutics to attenuate cardiac injury.

15 including ischemia/reperfusion (I/R)-induced cardiac injury.

16 sternal reentry is more likely to result in cardiac injury.

17 enotypes promotes excessive inflammation and cardiac injury.

18 ely used in clinics as a serum biomarker for cardiac injury.

19 milar protective effects against DOX-induced cardiac injury.

20 gnaling in a cardioprotective role following cardiac injury.

21 -adrenergic receptor agonist known to induce cardiac injury.

22 n unusual capacity to regenerate after acute cardiac injury.

23 radiation techniques may reduce the risk of cardiac injury.

24 el or sustained neovascularization following cardiac injury.

25 Angiopoietin-1 limits ischemia-induced cardiac injury.

26 ments for clinical or ECG signs of potential cardiac injury.

27 ceptibility of the HFE gene knockout mice to cardiac injury.

28 ric oxide and superoxide in various forms of cardiac injury.

29 e pathophysiological model of stroke-induced cardiac injury.

30 and Bl.Tg.Ealpha [IA+ IE+]) had substantial cardiac injury.

31 accumulation of Ca2+, has been implicated in cardiac injury.

32 itivity and specificity for the detection of cardiac injury.

33 a variety of experimental models of ischemic cardiac injury.

34 remodeling of gene expression in response to cardiac injury.

35 le in gap junction remodeling in response to cardiac injury.

36 e known to be a major target during ischemic cardiac injury.

37 gesting mitochondria as the critical site of cardiac injury.

38 the ENPP1/AMP pathway enhanced repair after cardiac injury.

39 his process in humans after various forms of cardiac injury.

40 both ischemia and reperfusion (I/R) causing cardiac injury.

41 that can cause debilitating and irreversible cardiac injury.

42 ing ATP and leading to energetic deficit and cardiac injury.

43 of extracellular matrix deposition following cardiac injury.

44 fic and rapid vessel margination response to cardiac injury.

45 expression in heart, brain and kidney after cardiac injury.

46 ases and is integral for regeneration during cardiac injury.

47 onverting enzyme-2 (p < 0.001) experienced a cardiac injury.

48 was positively correlated with the extent of cardiac injury.

49 g responses after ischaemic or non-ischaemic cardiac injury.

50 riving adaptive and maladaptive responses to cardiac injury.

51 mechanism to limit (m)Ca(2+) overload during cardiac injury.

52 luences cardiac tolerance and sensitivity to cardiac injury.

53 ed that PAI-1 also regulates fibrosis during cardiac injury.

54 a LOF both lead to unresolved scarring after cardiac injury.

55 oting endogenous revascularization following cardiac injury.

56 are capable of heart regeneration following cardiac injury.

57 e treatment of older patients suffering from cardiac injury.

58 omyocytes in vitro as well as in vivo during cardiac injury.

59 yte recruitment to the heart following acute cardiac injury.

60 ndent cardiac troponin elevation to indicate cardiac injury.

61 93 is important for tissue oxygenation after cardiac injury.

62 l and smooth muscle cells in vitro and after cardiac injury.

63 rtant regulators mediating their response to cardiac injury.

64 nt for the enhanced protective effects after cardiac injury.

65 n contributing to the detrimental effects of cardiac injury.

66 unt a strong regenerative response following cardiac injury.

67 phatics help to restore heart function after cardiac injury(1-6).

68 ung injury; 4) The role of exosomes in acute cardiac injury; 5) The role of exosomes in acute kidney

69 After cardiac injury, activated cardiac myofibroblasts can inf

70 Cardiac injury activates dynamic gene expression program

71 STAT3 are significantly more susceptible to cardiac injury after doxorubicin treatment than age-matc

72 diac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convinci

73 ical studies have shown that the severity of cardiac injury after myocardial infarction exhibits a ci

74 choice in screening patients for a possible cardiac injury after penetrating chest trauma by detecti

75 with non-small-cell lung cancer (NSCLC), yet cardiac injury after treatment is a significant concern.

76 ant, AAV.IR41, with enhanced transduction in cardiac injuries and with elevated transduction of TREE-

77 DN was associated with reduced biomarkers of cardiac injury and a 100% increase in cardiac viability

78 enerate intracellular Na+ and Ca2+ overload, cardiac injury and arrhythmia in the heart.

79 yocardium, is activated to proliferate after cardiac injury and can contribute vascular support cells

80 or pharmacological inhibition of IDO limits cardiac injury and cardiac dysfunction after MI.

81 Doxorubicin causes cardiac injury and cardiomyopathy in children with acute

82 tudying the role of alpha-E-catenin in human cardiac injury and cardiomyopathy in the future.

83 dualize treatment by immediately identifying cardiac injury and cardiomyopathy.

84 ance of studying the role of PINCHs in human cardiac injury and cardiomyopathy.

85 ed by altering cardiac parameters reflecting cardiac injury and cardiovascular disease, including hea

86 kine-dependent dysfunction during both acute cardiac injury and chronic cardiac pathologies.

87 an produce the serious side effects of acute cardiac injury and chronic congestive heart failure.

88 Among adults, cardiac injury and CV events are common post-CAR-T.

89 Potential cardiac injury and danger to viable grafts from repeated

90 or PINCH2 in myocardium leads to exacerbated cardiac injury and deterioration in cardiac function aft

91 based organ-on-a-chip models to recapitulate cardiac injury and dysfunction and for screening of card

92 rculating histone levels have been linked to cardiac injury and dysfunction in experimental models an

93 Cardiac injury and dysfunction occur in COVID-19 patient

94 is involved in the regulation of I/R-induced cardiac injury and dysfunction via antithetical regulati

95 Last, we review the models used to induce cardiac injury and essential ideas derived from studying

96 ne, a matrix metalloproteinase inhibitor, on cardiac injury and functional recovery in a swine model

97 lly increased cTnT may represent subclinical cardiac injury and have important clinical implications,

98 rol and GSK-3alpha KO mice were subjected to cardiac injury and heart parameters were evaluated.

99 gated the role of neuropilins in response to cardiac injury and heart regeneration.

100 imal elevations in biomarkers of subclinical cardiac injury and hemodynamic stress modify the associa

101 ion administration of doxycycline attenuates cardiac injury and improves functional recovery in newbo

102 perfusion correlates with the level of acute cardiac injury and involves rapid margination to the cor

103 ed by doxorubicin and also protected against cardiac injury and loss of function.

104 Here, we have found that cardiac injury and mortality in models of myocardial inf

105 Cardiac injury and myocarditis have been described in ad

106 Given the important role of cardiac injury and neurohormonal activation in the pathw

107 n early heart failure phenotypes, preventing cardiac injury and neurohormonal activation.

108 e of MI and redefine the CFs that respond to cardiac injury and participate in myocardial remodeling.

109 , is critical for control of immune-mediated cardiac injury and polymorphonuclear leukocyte inflammat

110 luronan, heparan sulfate) are upregulated on cardiac injury and regulate key processes in the remodel

111 d splenic T cells in HF are primed to induce cardiac injury and remodeling, and retain this memory on

112 Cardiac injury and remodelling are associated with the r

113 idence of new physiological phenomena during cardiac injury and repair as well as cardiac drug-mediat

114 in the infarcted heart; however, its role in cardiac injury and repair remains controversial.

115 al conditioning may result in a reduction of cardiac injury and support rapid recovery after major su

116 ion is an early event in doxorubicin-induced cardiac injury and that titin degradation occurs by acti

117 te NF-kappaB signaling as a key node between cardiac injury and tissue regeneration.

118 ed COVID-19 associated arrhythmic risks from cardiac injury and/or from pharmacotherapy such as the c

119 contribute importantly to remodeling during cardiac injury and/or inflammation.

120 Although markers of inflammation, cardiac injury, and coagulopathy have been previously as

121 o atherosclerosis, thrombosis, inflammation, cardiac injury, and fibrosis are introduced in the conte

122 g mitochondria Ca(2+) influx dynamics, acute cardiac injury, and long-term adaptation after ischemic

123 k stratification, diagnosis and prognosis of cardiac injury, and multiple forms of cardiovascular dis

124 ics in myeloid and fibroblast lineages after cardiac injury, and provide an entry point for deeper an

125 inical features, markers of inflammation and cardiac injury, and severe acute kidney injury.

126 ocyte mechanical interactions develop during cardiac injury, and that cardiac conduction may be impai

127 erexpression of Hsp20 inhibits DOX-triggered cardiac injury, and these beneficial effects appear to b

128 PKG Ialpha disulfide formation triggers cardiac injury, and this initiation of maladaptive signa

129 At the moment, the most specific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac

130 onavirus disease 2019 (COVID-19) who develop cardiac injury are reported to experience higher rates o

131 of symptomatic severe AS patients, stage of cardiac injury as classified by a novel staging system w

132 e virus revealed evidence of autoimmunity or cardiac injury as determined by T cell response to cardi

133 known to induce oxidative stress and thereby cardiac injury, as a model cardiotoxic compound and obse

134 Dexrazoxane prevents or reduces cardiac injury, as reflected by elevations in troponin T

135 cardiomyocytes to proliferate in response to cardiac injury, as well as transplantation of cardiomyoc

136 ocardium of diabetic rodents suggesting that cardiac injury associated with PKCbeta2 activation, diab

137 aluable in understanding the pathogenesis of cardiac injury associated with retroviral infection in a

138 Cardiac injury-associated biomarkers were more pronounce

139 mice that resulted in higher viral loads and cardiac injury at day 8 after infection.

140 Also, the response to cardiac injury at postnatal day 15 is intermediate betwe

141 stigated the influence of O-GlcNAc levels on cardiac injury at the cellular level.

142 x4 expression, indicating that AngII worsens cardiac injury, at least in part by enhancing Nox4 expre

143 ummarise the mechanisms of treatment-related cardiac injury, available clinical data, and protocols f

144 um measurements of cardiac troponin T (cTnT; cardiac injury biomarker), N-terminal pro-brain natriure

145 In contrast, four out of five postoperative cardiac injury biomarkers (NT-proBNP, H-FABP, hs-cTnT, a

146 of urine kidney injury biomarkers and plasma cardiac injury biomarkers in adverse events, we conducte

147 A significant increase in cardiac injury biomarkers was observed at 18-24 hours in

148 lammation, cytokine storm, and elevations of cardiac injury biomarkers.

149 ith the appearance of microscopic injury and cardiac injury biomarkers.

150 rophages are crucial for tissue repair after cardiac injury but are not well characterized.

151 cardiomyocyte origin is present during acute cardiac injury but has not been established as a biomark

152 ure is involved in the pathogenesis of acute cardiac injuries, but little is known about its role in

153 flammatory cytokines released in response to cardiac injury by chemotherapy or acute ischemia.

154 IF is expressed in cardiomyocytes and limits cardiac injury by enhancing AMPK activity during ischemi

155 mice/tandem dimer Tomato (tdTomato) mice to cardiac injury by permanent ligation of the left anterio

156 After acute cardiac injury, c-kit(+) cells retain their endothelial

157 r inflammation, neurohumoral activation, and cardiac injury can predict appropriate shocks and all-ca

158 After cardiac injury, cardiac progenitor cells are acutely red

159 n plasma levels of the clinical biomarker of cardiac injury, cardiac troponin-I, by 52+/-17% (P=1.01x

160 ncreased the myocyte resistance to the acute cardiac injury caused by enteroviral infection.

161 echanotransduction in mediating vascular and cardiac injury caused by the vascular endothelial growth

162 ac function or scar formation in response to cardiac injury compared with control mice.

163 antly increased CVB3 levels in the heart and cardiac injury compared with controls.

164 r rates of morbidity and mortality following cardiac injury compared with WT; however, adaptive cardi

165 indings suggest that bacterial pneumonia and cardiac injury contribute to fatal outcomes after infect

166 To treat cardiac injuries created by myocardial infarcts, current

167 rong myocardial tracer uptake in 2 models of cardiac injury (diphtheria toxin induced cardiomyocyte a

168 treatment of ischemia with genes that limit cardiac injury due to hypoxia.

169 Cardiac injury due to inadequate energy production from

170 role of MIF in regulating JNK activation and cardiac injury during experimental ischemia/reperfusion

171 ry circulation, and this resulted in greater cardiac injury during ischemia-reperfusion.

172 Induction of autophagy and cardiac injury during the reperfusion phase was signific

173 g ARDS, but the role of heart macrophages in cardiac injury during viral ARDS remains unknown.

174 Following cardiac injury, early immune cell responses are essentia

175 decreases in miR-101a levels at the onset of cardiac injury enhanced CM proliferation.

176 Prior studies of hepatic and cardiac injury examined limited repertoires of UPR eleme

177 ignificance of radiotherapy (RT) -associated cardiac injury for stage III non-small-cell lung cancer

178 d applied it to identify early biomarkers of cardiac injury from the blood of patients undergoing a t

179 The role of NHE1 in cardiac injury has prompted interest in the development

180 inding protein (HFABP) as an early marker of cardiac injury holds a promising future with studies ind

181 ge, which may in turn lead to a reduction in cardiac injury, hypertrophy, fibrosis, remodeling, and s

182 as that a sternotomy was unnecessary and the cardiac injury, if present, had sealed.

183 nervous system (SNS) overstimulation-evoked cardiac injuries in humans.

184 cribes a 10-min surgical procedure to induce cardiac injury in 1-d-old neonatal mice.

185 ve evaluated the association between HTN and cardiac injury in 388 COVID-19 (47.5 15.2 years) includi

186 diac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance spor

187 To investigate cardiac injury in borrelia carditis, we used antibody-de

188 : use of biomarkers for early recognition of cardiac injury in children receiving chemotherapy, devel

189 pertrophy (LVH) is an important mechanism of cardiac injury in CKD.

190 e basis for promoting regeneration following cardiac injury in human patients.

191 and promising therapeutic strategy to treat cardiac injury in humans.

192 Cardiac injury in mammals and amphibians typically leads

193 Cardiac injury in mice expressing cyclin D1 or D3 result

194 In contrast, cardiac injury in mice expressing cyclin D2 did not alte

195 le of ABCC6 in the calcification response to cardiac injury in mice.

196 mTOR complex 1 signaling attenuates diabetic cardiac injury in OVE26 mice.

197 ition, recent work examining the response to cardiac injury in the mammalian heart has suggested that

198 apoptosis plays a critical role in mediating cardiac injury in the setting of viral myocarditis and i

199 as increased in some mutant mice and reduced cardiac injury in these animals.

200 AAV-muUtro was highly protective against cardiac injury in these distinct models, evidenced by re

201 e coronary syndrome, indicating unrecognized cardiac injury in these settings.

202 This study shows that E. coli OMVs induce cardiac injury in vitro and in vivo, in the absence of b

203 on in proliferative cardiomyocytes following cardiac injury in zebrafish.

204 enhance mTORC1 activity may reduce diabetic cardiac injury, in sharp contrast to the results previou

205 rophages during obesity-hypertension-induced cardiac injury, including diastolic dysfunction and impa

206 mes in a mouse model of ischemia/reperfusion cardiac injury, indicating that optimized exemplars from

207 ays, play a pivotal role in the reduction of cardiac injury induced by mechanical stress or ischemia

208 Cardiac injury induced the expression of the ectonucleot

209 tive zebrafish and non-regenerative mammals, cardiac injury induces a sustained macrophage response.

210 It remains unclear whether cardiac injury influences sleep and whether sleep-mediat

211 ammatory and apoptotic responses may promote cardiac injury initiated by passively acquired autoantib

212 Acute cardiac injury is a common extrapulmonary manifestation

213 Post-burn cardiac injury is a common finding and predictor of mort

214 dings indicate that (1) beta-agonist-induced cardiac injury is associated with activation of the ASK1

215 Cardiac injury is common in asphyxiated neonates and is

216 Cardiac injury is common in patients who are hospitalize

217 of Grem2 and BMP-signaling inhibitors after cardiac injury is currently unknown.

218 In other organisms, such as zebrafish, cardiac injury is followed by transient fibrosis and sca

219 edge of molecular pathways connecting ROS to cardiac injury is lacking.

220 ectly contribute to neovascularization after cardiac injury is not known.

221 for the treatment of heart tissue damaged by cardiac injury is to develop strategies for restoring he

222 f COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown.

223 in regulating immune cell responses to acute cardiac injury is unknown.

224 er development of efficient therapeutics for cardiac injury, it is essential to uncover molecular mec

225 PK-DN mice subjected to MI/R endured greater cardiac injury (larger infarct size, more apoptosis, and

226 njury, excessive hemorrhage, and inadvertent cardiac injury leading to morbidity and mortality.

227 Cardiac injury leads to the loss of cardiomyocytes, whic

228 Genetic ablation of MMP-9 attenuated cardiac injury, left ventricle dilation, and fibrosis in

229 unit clinician, including new biomarkers of cardiac injury like troponin T and I.

230 hol-induced cardiac fibrosis and more severe cardiac injury, making the MT-KO mouse model of alcohol-

231 2b2 vaccination, genistein treatment reduced cardiac injury markers and attenuated infiltration of ne

232 In addition, cardiac injury markers such as creatine kinase (CK), myo

233 Serial measurements of cardiac injury markers were not obtained.

234 Demographic data, cardiac injury markers, other laboratory findings, and c

235 Acute cardiac injury may be associated with whether the virus

236 Several components of the cardiac injury microenvironment have been identified, ye

237 We sought to determine whether subclinical cardiac injury might also occur in acute liver failure.

238 A murine cardiac injury model was performed by subcutaneous infus

239 oducible pharmacologic- and exercise-induced cardiac injury models in the mdx mouse and rigorous test

240 In contrast, data analyses for mammalian cardiac injury models indicated that inflammation and me

241 s or via cell transplantation in preclinical cardiac injury models.

242 ted in communication defects associated with cardiac injury, namely arrhythmogenesis and progression

243 ch incorporating assessment of extravalvular cardiac injury, novel imaging markers, and biomarkers is

244 , and albumin) and five plasma biomarkers of cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK

245 Acute cardiac injury occurs in half of critically ill coronavi

246 (93%) randomized to sternotomy had either no cardiac injury or a tangential injury.

247 Although rare instances of cardiac injury or arrhythmias have been reported in acut

248 death in the western world, develops when a cardiac injury or insult impairs the ability of the hear

249 2 hours post-MI but had no effect on initial cardiac injury or structure.

250 factor (CTGF) is upregulated in response to cardiac injury or with transforming growth factor beta (

251 ission levels of biomarkers of inflammation, cardiac injury, or fibrinolysis.

252 roptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and hea

253 artery disease reduced renal dysfunction and cardiac injury, potentially resulting in improved surviv

254 Fibrosis resulting from cardiac injury presents a major challenge to restoring h

255 the epicardium becomes dormant after birth, cardiac injury reactivates developmental gene programs t

256 Because the mammalian heart scars following cardiac injury, recent work showing that cardiac fibrobl

257 gonucleotide miR-494 increased I/R-triggered cardiac injury relative to the administration of mutant

258 Cardiac injury remains a major cause of morbidity and mo

259 cardiac remodeling, but its precise role in cardiac injury remains controversial.

260 dings indicate that epicardium modulates the cardiac injury response by conditioning the subepicardia

261 lpha (Mapk14 gene) is known to influence the cardiac injury response, but its direct role in orchestr

262 Cardiac injury resulted in a approximately 6.45-fold exp

263 mine whether fibroblast activation following cardiac injury results in a distinct electrophysiologica

264 These data demonstrate cardiac injury results in significant electrophysiologic

265 a subgroup of patients with more complicated cardiac injuries such as coronary artery injuries, septa

266 nt of mesenchymal stem cells (MSC) following cardiac injury, such as myocardial infarction, plays a c

267 Experiments in mammalian models of cardiac injury suggest that the cardiomyocyte-specific o

268 emic inflammatory diseases, cancer, and post-cardiac injury syndromes).

269 cular system, including causing irreversible cardiac injury that can result in reduced quality of lif

270 lating exosomes allow a systemic response to cardiac injury that may be leveraged for cardiac repair.

271 In response to cardiac injury the mammalian heart undergoes ventricular

272 Following cardiac injury, the epicardium is activated organ-wide i

273 yocytes can reenter the cell cycle following cardiac injury, the myocardium is largely thought to be

274 ficiency and Stat3 deficiency both aggravate cardiac injury through their regulation on the MR/FGF21

275 evels correlated with established markers of cardiac injury, thus uncovering the presence of subclini

276 ferative expansion, transforming subclinical cardiac injury to overt heart failure.

277 proliferation of spared cardiomyocytes after cardiac injury to regenerate lost heart muscle.

278 ith a penetrating chest wound and a possible cardiac injury to the Groote Schuur Hospital Trauma Cent

279 with troponin-I, the conventional marker of cardiac injury, to add diagnostic information in chest p

280 Cardiac injury triggers the generation of bioactive TGFb

281 l and erythrocyte sedimentation rate [ESR]), cardiac injury (troponin level), and fibrinolysis (D-dim

282 Acute ischaemic cardiac injury upregulates Wnt1 that is initially expres

283 nd implications for therapeutically relevant cardiac injury versus cardiac repair.

284 Cardiac injury was decreased in CPNS1 deletion mice foll

285 s a biomarker of doxorubicin-induced chronic cardiac injury was evaluated in the spontaneously hypert

286 Cardiac injury was independently associated with signifi

287 Cardiac injury was induced in neonatal and adult hearts

288 Cardiac injury was induced in the adult feline heart by

289 e cardiomyocyte proliferative response after cardiac injury was lost in G3 Terc(-/-) newborns but res

290 id libraries dosed systemically in mice post-cardiac injury, we discovered a new capsid variant, AAV.

291 n of transgenes in border zone regions after cardiac injury when packaged into recombinant adeno-asso

292 ad to a possible false-positive diagnosis of cardiac injury when skeletal muscle pathology is present

293 is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and redu

294 ssociated with diagnoses related to ischemic cardiac injury while HFpEF was associated more with non-

295 3 nm); two greatly reduced ischemia-induced cardiac injury with an IC50 of approximately 200 nm and

296 Cardiac injury with attendant negative prognostic implic

297 presentations but often presents as an acute cardiac injury with cardiomyopathy, ventricular arrhythm

298 We investigated the role of CTRP9 in cardiac injury with loss-of-function genetic manipulatio

299 neumoniae invades the myocardium and induces cardiac injury with necroptosis and apoptosis, followed

300 of immune cell localization following acute cardiac injury, with deficient leukocyte infiltration in