首页> 外文期刊>Frontiers in Neurology >Peptidylarginine Deiminases as Drug Targets in Neonatal Hypoxic–Ischemic Encephalopathy
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Peptidylarginine Deiminases as Drug Targets in Neonatal Hypoxic–Ischemic Encephalopathy

机译:肽酰精氨酸去氨酶作为新生儿缺氧缺血性脑病的药物靶点

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Oxygen deprivation and infection are major causes of perinatal brain injury leading to cerebral palsy and other neurological disabilities. The identification of novel key factors mediating white and gray matter damage are crucial to allow better understanding of the specific contribution of different cell types to the injury processes and pathways for clinical intervention. Recent studies in the Rice–Vannucci mouse model of neonatal hypoxic ischemia (HI) have highlighted novel roles for calcium-regulated peptidylarginine deiminases (PADs) and demonstrated neuroprotective effects of pharmacological PAD inhibition following HI and synergistic infection mimicked by lipopolysaccharide stimulation.
机译:缺氧和感染是围产期脑损伤的主要原因,导致脑瘫和其他神经系统疾病。鉴定介导白质和灰质损伤的新关键因子对于更好地了解不同细胞类型对损伤过程和临床干预途径的特定贡献至关重要。 Rice-Vannucci新生鼠缺氧缺血(HI)小鼠模型中的最新研究突出了钙调节肽基精氨酸脱氨酶(PADs)的新作用,并证实了HI和脂多糖刺激模拟的协同感染后药理PAD抑制的神经保护作用。

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