Molecular mechanisms of signaling via the docosanoid neuroprotectin D1 for cellular homeostasis and neuroprotection.
Molecular mechanisms of signaling via the docosanoid neuroprotectin D1 for cellular homeostasis and neuroprotection.
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DOI：
10.1074/jbc.r117.783076
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发表时间：
2017-07-28
期刊：
影响因子：
--
通讯作者：
Bazan NG
中科院分区：
文献类型：
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作者：
Asatryan A;Bazan NG
二十二碳六烯酸，富含在大脑和视网膜中，产生二十二碳二烯类化合物，以应对细胞内稳态的破坏。Docosanoid包括神经保护素D1(NPD1)，它在早期阿尔茨海默病(AD)患者的CA1海马区减少。我们在这里总结了NPD1是如何通过上调c-Rel来发挥神经保护作用的，c-Rel是一种核因子(NF)-κB亚型，反过来又增强了BIRC3(杆状病毒抑制凋亡重复序列包含蛋白3)在视网膜和实验性中风中的表达，从而导致神经保护。阐明二十二碳二烯类化合物的作用机制将有助于控制疾病，包括中风、AD、老年性黄斑变性、创伤性脑损伤、帕金森病和其他神经退行性疾病。
Docosahexaenoic acid, enriched in the brain and retina, generates docosanoids in response to disruptions of cellular homeostasis. Docosanoids include neuroprotectin D1 (NPD1), which is decreased in the CA1 hippocampal area of patients with early-stage Alzheimer's disease (AD). We summarize here how NPD1 elicits neuroprotection by up-regulating c-REL, a nuclear factor (NF)-κB subtype that, in turn, enhances expression of BIRC3 (baculoviral inhibitor of apoptosis repeat-containing protein 3) in the retina and in experimental stroke, leading to neuroprotection. Elucidating the mechanisms of action of docosanoids will contribute to managing diseases, including stroke, AD, age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other neurodegenerations.