2015
DOI: 10.1016/j.jstrokecerebrovasdis.2015.03.032
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Human Urinary Kallidinogenase Improves Outcome of Stroke Patients by Shortening Mean Transit Time of Perfusion Magnetic Resonance Imaging

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Cited by 26 publications
(26 citation statements)
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“…After treatment with HUK, AIS patents' cerebral blood perfusion was significantly enhanced and mean transit time of perfusion was remarkably shorten, which are in accordance with increasing serum levels of VEGF and apelin ( 16 ). These two substances are all involved in vascular formation and maturation ( 17 , 18 ).…”
Section: Results From Clinical Trialssupporting
confidence: 52%
“…After treatment with HUK, AIS patents' cerebral blood perfusion was significantly enhanced and mean transit time of perfusion was remarkably shorten, which are in accordance with increasing serum levels of VEGF and apelin ( 16 ). These two substances are all involved in vascular formation and maturation ( 17 , 18 ).…”
Section: Results From Clinical Trialssupporting
confidence: 52%
“…95 A small, open-label, controlled, prospective study implied that short-term application of human urinary kallidinogenase could upregulate vascular endothelial growth factor and apelin expression, shorten the MTT in MR perfusion, and improve the 3-month functional outcome, as compared with control, among patients with acute stroke. 96 According to a systematic review and meta-analysis of 24 trials with 2433 patients published in 2012, human urinary kallidinogenase injection reduced death or dependency in two trials (RR 0.69; 95% CI 0.55 to 0.86) and increased the rate of neurological improvement after treatment based on data from 20 trials (2117 patients) (RR 1.56; 95% CI 1.44 to 1.70) as compared with control, while the risks of non-fatal intracranial haemorrhage or death were not significantly different between those treated with human urinary kallidinogenase or controls. 97 …”
Section: Interventions To Enhance Cerebral Collateral Circulation In mentioning
confidence: 99%
“…Recent studies suggest that apelin-13 protects the neurovascular unit against ischemic injuries, which is dependent on an increase of VEGF-VEGF receptor 2 (VEGFR2) signaling, possibly by activating ERK and PI3K/AKT pathways (51). Moreover, the apelin/APJ system may work in coordination with VEGF to trigger vascular sprouting and CBF recovery from human urinary kallidinogenase (HUK)treated stroke patients in an ERK1/2-dependent manner (91,92). On the contrary, the expression of VEGF in cultured endothelial cells is partially suppressed by the apelin/APJ system inhibitor, suggesting that the apelin/APJ system may cooperate with VEGF to promote vascular growth in ischemic stroke (92).…”
Section: Promoting Angiogenesismentioning
confidence: 99%