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1 iators which are generated during myocardial ischemic injury.
2 and meningeal IL-17(+) gammadelta T cells on ischemic injury.
3 to attenuate cell death and protect against ischemic injury.
4 ntioxidant and neuroprotective agent against ischemic injury.
5 ccompanied by increased infarct volume after ischemic injury.
6 supports tubular proliferation after sterile ischemic injury.
7 ction, and impairment of tissue repair after ischemic injury.
8 es in intracellular compartments after renal ischemic injury.
9 ion abolished the increase of 5hmC caused by ischemic injury.
10 ed the myocardial leukocyte population after ischemic injury.
11 PUFA is sufficient to protect the liver from ischemic injury.
12 ule (PT) cells are critical targets of acute ischemic injury.
13 he receptor and ligand are upregulated after ischemic injury.
14 r impact and the impact of Candq1, alone, on ischemic injury.
15 a in neurons and are protected from cerebral ischemic injury.
16 candidate to limit neuronal apoptosis after ischemic injury.
17 n and prevention of fibrosis following acute ischemic injury.
18 survival and reparative proliferation after ischemic injury.
19 during storage may influence the severity of ischemic injury.
20 thways can be beneficial in the treatment of ischemic injury.
21 potential therapeutic for combating cardiac ischemic injury.
22 g proteotoxicity and heart dysfunction after ischemic injury.
23 ffers a means to protect the myocardium from ischemic injury.
24 l conditions, correlating with the degree of ischemic injury.
25 itioning, is not associated with ischemia or ischemic injury.
26 hancing AMPK activation and reducing cardiac ischemic injury.
27 long-term regional visual field loss due to ischemic injury.
28 ogical changes and cell death during cardiac ischemic injury.
29 e molecular pattern molecules released after ischemic injury.
30 this cardiac mitochondrial subpopulation on ischemic injury.
31 role in determining the severity of cerebral ischemic injury.
32 death signaling and neuroprotection against ischemic injury.
33 e remnant nephrons precondition them against ischemic injury.
34 kidneys have been subjected to warm or cold ischemic injury.
35 ac remodeling and function in the setting of ischemic injury.
36 memory and in protection of neurons against ischemic injury.
37 kineticin 2 (PK2) as a mediator for cerebral ischemic injury.
38 of cardiac autophagy and displayed increased ischemic injury.
39 activation and proliferation in response to ischemic injury.
40 esearch by serving as a surrogate measure of ischemic injury.
41 disruption of blood supply which results in ischemic injury.
42 iac fibrosis, and in myocardial responses to ischemic injury.
43 ars, regulates the size of heart scars after ischemic injury.
44 t has therapeutic potential to prevent renal ischemic injury.
45 s of the lectin complement pathway, in brain ischemic injury.
46 miRNAs to therapeutically inhibit miR-15 on ischemic injury.
47 beneficial effects on outcome after hypoxic-ischemic injury.
48 ess and an endogenous repair mechanism after ischemic injury.
49 s rapidly and greatly following traumatic or ischemic injury.
50 lerated long-term in eyes with acute retinal ischemic injury.
51 arction, a model of acute inflammation after ischemic injury.
52 ole in protecting lean and fatty livers from ischemic injury.
53 epresent one of the brain's defenses against ischemic injury.
54 EC, which promotes cardioprotection against ischemic injury.
55 d to the repair and recovery phase following ischemic injury.
56 ve responses in adult and neonatal models of ischemic injury.
57 target for preventing muscle fibrosis after ischemic injury.
58 a variety of diseases ranging from cancer to ischemic injury.
59 n the setting of a severe form of myocardial ischemic injury.
60 protein S (PS) protects neurons from hypoxic/ischemic injury.
61 st predictive when combined with presence of ischemic injury.
62 model play a role in vessel formation after ischemic injury.
63 ng HDAC activity can protect the retina from ischemic injury.
64 orrhages, and 35 (35%) had evidence of acute ischemic injury.
65 nduces tolerance against a subsequent lethal ischemic injury.
66 itigate adverse ventricular remodeling after ischemic injury.
67 is present in the heart and activated after ischemic injury.
68 s for skeletal muscle regeneration following ischemic injury.
69 n Thy1Cre;EP2(lox/lox) mice reduced cerebral ischemic injury.
70 sh kidney tissue, and urine before and after ischemic injury.
71 signaling through ERK and Akt in response to ischemic injury.
72 thological mechanism that led to the initial ischemic injury.
73 of the heart following both ischemic and non-ischemic injury.
74 ulation enhanced interstitial fibrosis after ischemic injury.
75 ar (caSMC and caEC) mechanisms in myocardial ischemic injury.
76 e where a global deletion increases cerebral ischemic injury.
77 stress and protects the brain and heart from ischemic injury.
78 d to reduce cellular metabolism and minimize ischemic injury.
79 l entities, discovering a small molecule for ischemic injury.
80 ioprotective capabilities against myocardial ischemic injury.
81 ox9 blunted the cardiac fibrotic response on ischemic injury.
82 rdiac injury, and long-term adaptation after ischemic injury.
83 tion to the intercalated discs against acute ischemic injury.
84 to allow sufficient tissue reperfusion after ischemic injury.
85 es that become activated under conditions of ischemic injury.
86 nt of therapeutics to protect the brain from ischemic injury.
87 fibrin microthrombi, without universal acute ischemic injury.
88 e neuroprotective strategy to treat cerebral ischemic injury.
89 he regenerative capacity even in spite of an ischemic injury.
90 r and regenerate the damaged myocardium from ischemic injury.
91 metabolism, induce apoptosis, and exacerbate ischemic injury.
92 ammation and leukocyte recruitment following ischemic injury.
93 it is also a major pathomechanism underlying ischemic injury.
94 p53 may facilitate muscle regeneration after ischemic injuries.
95 eutic target for treating complications from ischemic injuries.
96 yocyte cell death following ischemic and non-ischemic injuries.
97 cognitive benefits in the context of hypoxic-ischemic injuries.
98 and quality of life of patients with severe ischemic injuries.
100 ) were hemorrhagic transformation of primary ischemic injuries (14 with neonatal cerebral sinovenous
101 protected from both transient and permanent ischemic injury; (2) Polyman2, the newly synthesized man
102 noid hemorrhage (4/80; 5%) or global hypoxic-ischemic injury (20/202, 10%) were more likely to achiev
103 ng repair and recovery of function following ischemic injury, a knock-in (KI) mouse expressing the UC
109 o a novel treatment option that can decrease ischemic injury after traumatic brain injury without inc
111 ia protects the rodent brain from subsequent ischemic injury, although the protection wanes within da
113 ular protons produced during inflammation or ischemic injury and belong to the superfamily of degener
114 regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inh
115 ; for example, miR-214 is upregulated during ischemic injury and heart failure, but its potential rol
117 regulation of emergency hematopoiesis after ischemic injury and identify potential therapeutic targe
118 he one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial
120 (FSTL1) is a cardioprotective factor against ischemic injury and is induced in cardiomyocytes and ske
122 ment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effec
123 spects of the natural protective response to ischemic injury and may be novel therapeutic targets for
124 rom bone marrow niches in response to remote ischemic injury and migrate to the areas of damage and s
127 lecular pathways that regulate the extent of ischemic injury and post-myocardial infarction (MI) remo
129 of insulin signaling, which increases after ischemic injury and precedes heart failure development.
130 zation of cardiac vasculature that mitigated ischemic injury and predicted outcomes after myocardial
131 nt role for MBL in the pathogenesis of brain ischemic injury and provide a strong support to the conc
132 Remarkably, mAPC(PS/N329Q) limited cerebral ischemic injury and reduced brain lesion volume signific
133 st, when genetic labeling was induced during ischemic injury and subsequent recovery, the number of l
134 rain during the recovery phase from an acute ischemic injury and that uPA binding to uPAR promotes ne
135 ropriate methods to assess risk for cerebral ischemic injury and the relationship of intradialytic ce
136 protection to minimize procedure-associated ischemic injury and to improve outcomes of revasculariza
138 ed vascular regeneration in a mouse model of ischemic injury and were resistant to tumorigenic transf
139 xymethylated regions (DhMRs) associated with ischemic injury, and DhMRs were enriched among the genes
140 strate dendrimer uptake in cells involved in ischemic injury, and in ongoing inflammation, leading to
141 al hemorrhage, hemorrhagic transformation of ischemic injury, and presumed perinatal hemorrhagic stro
142 show that 5hmC abundance was increased after ischemic injury, and Tet2 was responsible for this incre
143 ammatory pathways to protect neurons against ischemic injury, and these beneficial effects of IF are
144 cells in the CNS) also express EPO following ischemic injury, and this response is known to ameliorat
145 is often taking medications that may affect ischemic injury; and (5) animal studies may not involve
146 ignals that activate the inflammasome during ischemic injury are not well characterized, we show that
147 ection of the brain from a subsequent severe ischemic injury, as induced by middle cerebral artery oc
149 ls, resulting in lower perfusion and greater ischemic injury at all time points over 21 days followin
151 identify that transvalvular unloading limits ischemic injury before reperfusion, improves myocardial
152 ls versus brain resident cells contribute to ischemic injury, bone marrow chimeras were generated by
153 orm-specific inhibition of GSK-3 exacerbates ischemic injury but protects against I/R injury by modul
154 Antioxidant therapy can protect against ischemic injury, but the inability to selectively target
155 d during renal epithelial regeneration after ischemic injury, but the molecular signals that control
156 lts demonstrated that EA attenuated cerebral ischemic injury by inhibiting NAPDH oxidase-mediated oxi
157 ocker, capsaicin, suggesting that RIP blocks ischemic injury by modulating protein synthesis and nerv
158 Organotypic cortical brain slices exposed to ischemic injury by oxygen-glucose deprivation were treat
159 these results indicate miR-24 promotes renal ischemic injury by stimulating apoptosis in endothelial
163 eeded resource, tissue damage from prolonged ischemic injury can result in early allograft dysfunctio
167 these compounds were evaluated further in an ischemic injury cell survival assay and a reactive oxyge
171 whether DCD livers with steatotic and severe ischemic injury could be discriminated from 'transplanta
172 ed susceptibility of early maturing axons to ischemic injury described here may significantly contrib
173 alysis may be at increased risk for cerebral ischemic injury disease due to vasculopathy associated w
175 y determination-of-death (DCD) donors suffer ischemic injury during a preextraction period of cardiac
176 suggests that female rats are vulnerable to ischemic injury during exposure and manipulation of the
177 will examine the utility in preventing post-ischemic injury during renal transplantation, where acut
180 integrity can be reversible in traumatic and ischemic injuries, highlighting mitochondria as a potent
182 repair or regeneration of tissues suffering ischemic injury, however clinical translation is limited
183 stem cells (MSCs) is a promising therapy for ischemic injury; however, inadequate survival of implant
184 ly regulates adult muscle regeneration after ischemic injury, implying that it coordinates adult myog
185 therapies to offset cardiomyocyte loss after ischemic injury improve long-term cardiac function despi
186 ate and identify molecular patterns of early ischemic injury in a clinically acceptable time frame.
187 icits tolerance to subsequent lethal hypoxic/ischemic injury in a natural process known as ischemic p
188 n shown to improve myocardial function after ischemic injury in animal models and in early clinical e
189 in vivo, leading to an improved response to ischemic injury in animal models of hindlimb ischemia.
190 rdiac remodeling and infarct expansion after ischemic injury in association with greater mitochondria
191 ffect of electroacupuncture (EA) on cerebral ischemic injury in diabetic mice, and explored the role
194 ter neuronal damage following focal cerebral ischemic injury in many experimental injury models, howe
195 ese two factors conferred protection against ischemic injury in mature mouse hearts that were otherwi
200 a role as a therapeutic agent to counteract ischemic injury in neural, cardiac and endothelial cells
206 e of extracellular adenosine triphosphate in ischemic injury in specific organs, in order to provide
207 kt1 was proposed as a therapeutic target for ischemic injury in the context of myocardial infarction
208 t role in cardiac myocyte protection against ischemic injury in the heart and supports the idea that
209 We induced type 2 myocardial infarction-like ischemic injury in the heart by treatment with a single
213 ver, the therapeutic role of gAD in cerebral ischemic injury in type 1 diabetes mellitus (T1DM) remai
214 This finding is physiologically relevant as ischemic injury in vivo provoked identical TLR4 response
215 1A, could lead to neuroprotection following ischemic injury in vivo The minimal syntaxin 1A-binding
217 ring chronic stroke, weeks after the initial ischemic injury, in male Sprague-Dawley rats via intrasp
218 suggested to improve cardiac function after ischemic injury, in particular by promoting neovasculari
221 A machine learning algorithm (myocardial-ischemic-injury-index [MI(3)]) incorporating age, sex, a
223 of miR-592 in neurons decreases the level of ischemic injury-induced p75(NTR) and attenuates activati
225 esence of MH at SW imaging-followed by acute ischemic injury, initial Glasgow Coma Scale score, and a
228 demonstrate that induction of p75(NTR) after ischemic injury is independent of transcription but requ
231 ha mediates the cardioprotective response to ischemic injury, its upregulation may be an effective th
234 arly, inflammatory phase of acute myocardial ischemic injury, Ly-6C(high) monocytes accrue in respons
235 ring the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have bee
236 ays after stroke and thus further exacerbate ischemic injury, manipulating its function presents a un
238 lphaKlotho upregulates autophagy, attenuates ischemic injury, mitigates renal fibrosis, and retards A
240 dialysis (HD) results in recurrent segmental ischemic injury (myocardial stunning) that drives cumula
241 gical conditions including myocardial aging, ischemic injury, myocardial fibrosis, and cardiomyocyte
243 cted to assess the protective effect against ischemic injury of a preservative solution supplemented
245 that miRNAs are dysregulated in response to ischemic injury of the heart and actively contribute to
246 important role in the pathogenesis of acute ischemic injury of the kidney, although possibly through
248 roblasts and ensuing fibrosis in response to ischemic injury or chronic neurohumoral stimulation.
250 delivery of EPCs protects the brain against ischemic injury, promotes neurovascular repair, and impr
251 vestigate whether HDAC inhibition can reduce ischemic injury, rats were treated with TSA (2.5 mg/kg i
256 chimera experiments determined that maximal ischemic injury required IRF-1 expression by both leukoc
258 ed EF, rather than HFpEF, secondary to acute ischemic injury resulting in myocardial infarction, and
259 ee distinct M-channel openers at 0-6 h after ischemic injury significantly decreased brain infarct si
261 the proliferation of tubular cells following ischemic injury, suggesting that they may have a role in
262 , initial response to invading pathogens and ischemic injury, sustained plasma cell growth, and immun
264 xhibit infarct size and heart function after ischemic injury that is similar to that of control mice.
265 e show in both ex vivo and in vivo models of ischemic injury that treatment with GLP-1(28-36), a neut
266 s early loss of axons results from a primary ischemic injury that triggers a wave of calcium signalin
267 ndogenous opioid receptor-activation reduces ischemic injury, the effects of the opioid antagonist na
268 ter the great success of therapies to reduce ischemic injury, the time has come to focus efforts on t
269 can confer acute protection against cardiac ischemic injury, their mechanism of action is unclear.
270 ility of the adult heart to regenerate after ischemic injury, there is a great opportunity to identif
271 hat makes cells and organs more resistant to ischemic injury, thereby extending the time they can tol
272 endogenous histones function as DAMPs after ischemic injury through the pattern recognition receptor
276 d permeability transition pore opening after ischemic injury to reduce ongoing pathological remodelin
279 ection, and cognitive preservation following ischemic injury to the brain.SIGNIFICANCE STATEMENT Foll
280 activation, and neuroprotection following an ischemic injury to the brain.SIGNIFICANCE STATEMENT Foll
286 tabilization in the first 6-24 h after renal ischemic injury was significantly reduced in mice lackin
287 her organ vulnerable to hemodialysis-induced ischemic injury, we also used echocardiography to assess
288 increase in superoxide contributes to renal ischemic injury, we created the folate-antioxidant conju
289 ther investigating the role of the spleen in ischemic injury, we found that prior splenectomy (-7d) o
290 nd the contribution of neuronal PPARgamma to ischemic injury, we generated conditional neuron-specifi
291 (-/-) and pifithrin-alpha-treated mice after ischemic injury were the anti-inflammatory M2 phenotype.
292 Nonocclusive fibrin microthrombi (without ischemic injury) were identified in 16 cases (12 COVID-1
293 d are capable of being recruited to sites of ischemic injury where they contribute to neovascularizat
294 he systemic circulation and home to sites of ischemic injury where they promote neoangiogenesis.
295 hy in the newborn heart can exacerbate these ischemic injuries, which may partly be due to a decrease
296 usly evaluate multiple vascular responses to ischemic injury, which can be useful in improving our un
297 received limited success in the treatment of ischemic injury, which include therapeutics against exci
298 ular capillaries (PTCs), promoting secondary ischemic injury, which may be central to disease progres
299 blood (HUCB) cells protect the brain against ischemic injury, yet the mechanism of protection remains
300 Effective progenitor cell recruitment to the ischemic injury zone is a prerequisite for any potential