Suppr超能文献

肽基精氨酸脱亚氨酶作为新生儿缺氧缺血性脑病的药物靶点

Peptidylarginine Deiminases as Drug Targets in Neonatal Hypoxic-Ischemic Encephalopathy.

作者信息

Lange Sigrun

机构信息

Department of Pharmacology, UCL School of Pharmacy, London, UK; Department of Biomedical Sciences, University of Westminster, London, UK.

出版信息

Front Neurol. 2016 Feb 22;7:22. doi: 10.3389/fneur.2016.00022. eCollection 2016.

Abstract

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.

摘要

缺氧和感染是导致围产期脑损伤进而引发脑瘫和其他神经残疾的主要原因。识别介导白质和灰质损伤的新关键因素对于更好地理解不同细胞类型对损伤过程的具体作用以及临床干预途径至关重要。最近在新生小鼠缺氧缺血(HI)的莱斯-万努奇模型中的研究突出了钙调节肽基精氨酸脱氨酶(PADs)的新作用,并证明了HI后药物性抑制PAD以及脂多糖刺激模拟协同感染后的神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31a5/4761975/a514975575a5/fneur-07-00022-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验