氧化应激与内质网应激在新生儿缺氧缺血性脑损伤发生发展中的作用
Oxidative stress and endoplasmic reticulum (ER) stress in the development of neonatal hypoxic-ischaemic brain injury.
作者信息
Thornton Claire, Baburamani Ana A, Kichev Anton, Hagberg Henrik
机构信息
Perinatal Brain Injury Group, Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King's College London, King's Health Partners, St. Thomas' Hospital, London SE1 7EH, U.K.
Perinatal Center, Institute of for Clinical Sciences and Physiology and Neurosciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg 41685, Sweden.
出版信息
Biochem Soc Trans. 2017 Oct 15;45(5):1067-1076. doi: 10.1042/BST20170017. Epub 2017 Sep 22.
Birth asphyxia in term neonates affects 1-2/1000 live births and results in the development of hypoxic-ischaemic encephalopathy with devastating life-long consequences. The majority of neuronal cell death occurs with a delay, providing the potential of a treatment window within which to act. Currently, treatment options are limited to therapeutic hypothermia which is not universally successful. To identify new interventions, we need to understand the molecular mechanisms underlying the injury. Here, we provide an overview of the contribution of both oxidative stress and endoplasmic reticulum stress in the development of neonatal brain injury and identify current preclinical therapeutic strategies.
足月儿出生窒息发生率为1-2/1000活产儿，可导致缺氧缺血性脑病，造成终身严重后果。大多数神经元细胞死亡会延迟发生，这为采取治疗措施提供了潜在的治疗窗口期。目前，治疗选择仅限于治疗性低温，但并非普遍有效。为了确定新的干预措施，我们需要了解损伤背后的分子机制。在此，我们概述了氧化应激和内质网应激在新生儿脑损伤发展中的作用，并确定了当前的临床前治疗策略。
Zotero 插件