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Mice with disrupted mitochondria used to model Parkinson's disease.

作者信息

Doric Zak, Nakamura Ken

出版信息

Nature. 2021 Nov;599(7886):558-560. doi: 10.1038/d41586-021-02955-z.

DOI:10.1038/d41586-021-02955-z
PMID:34732876
Abstract
摘要

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1
Mice with disrupted mitochondria used to model Parkinson's disease.线粒体功能紊乱的小鼠被用于帕金森病的模型构建。
Nature. 2021 Nov;599(7886):558-560. doi: 10.1038/d41586-021-02955-z.
2
Understanding the susceptibility of dopamine neurons to mitochondrial stressors in Parkinson's disease.了解帕金森病中多巴胺能神经元对线粒体应激源的易感性。
FEBS Lett. 2015 Dec 21;589(24 Pt A):3702-13. doi: 10.1016/j.febslet.2015.10.021. Epub 2015 Oct 23.
3
Neuronal complex I deficiency occurs throughout the Parkinson's disease brain, but is not associated with neurodegeneration or mitochondrial DNA damage.帕金森病大脑中存在神经元复合物 I 缺陷,但与神经退行性变或线粒体 DNA 损伤无关。
Acta Neuropathol. 2018 Mar;135(3):409-425. doi: 10.1007/s00401-017-1794-7. Epub 2017 Dec 21.
4
Mitochondria in Neuronal Health: From Energy Metabolism to Parkinson's Disease.神经元健康中的线粒体:从能量代谢到帕金森病
Adv Biol (Weinh). 2021 Sep;5(9):e2100663. doi: 10.1002/adbi.202100663. Epub 2021 Aug 11.
5
Is Bax a mitochondrial mediator in apoptotic death of dopaminergic neurons in Parkinson's disease?Bax是否是帕金森病中多巴胺能神经元凋亡死亡的线粒体介质?
J Neurochem. 2001 Mar;76(6):1785-93. doi: 10.1046/j.1471-4159.2001.00160.x.
6
The multi-faceted role of mitochondria in the pathology of Parkinson's disease.线粒体在帕金森病病理中的多方面作用。
J Neurochem. 2021 Mar;156(6):715-752. doi: 10.1111/jnc.15154. Epub 2020 Sep 20.
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Mitochondrial Metabolism Regulates Microtubule Acetylome and Autophagy Trough Sirtuin-2: Impact for Parkinson's Disease.线粒体代谢通过 Sirtuin-2 调节微管乙酰化组和自噬:对帕金森病的影响。
Mol Neurobiol. 2018 Feb;55(2):1440-1462. doi: 10.1007/s12035-017-0420-y. Epub 2017 Feb 6.
8
Mitochondria-targeted antioxidants for treatment of Parkinson's disease: preclinical and clinical outcomes.用于治疗帕金森病的线粒体靶向抗氧化剂:临床前和临床结果
Biochim Biophys Acta. 2014 Aug;1842(8):1282-94. doi: 10.1016/j.bbadis.2013.09.007. Epub 2013 Sep 20.
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Mouse models of Parkinson's disease associated with mitochondrial dysfunction.帕金森病相关的线粒体功能障碍的小鼠模型。
Mol Cell Neurosci. 2013 Jul;55:87-94. doi: 10.1016/j.mcn.2012.08.002. Epub 2012 Aug 11.
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Dopaminergic neurons reduced to silence by oxidative stress: an early step in the death cascade in Parkinson's disease?多巴胺能神经元因氧化应激而沉默:帕金森病死亡级联反应的早期步骤?
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Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.中脑多巴胺神经元的慢性过度激活会导致多巴胺神经元优先变性。
Elife. 2025 Aug 26;13:RP98775. doi: 10.7554/eLife.98775.
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The cholesterol 24-hydroxylase CYP46A1 promotes α-synuclein pathology in Parkinson's disease.胆固醇24-羟化酶CYP46A1促进帕金森病中的α-突触核蛋白病理改变。
PLoS Biol. 2025 Feb 18;23(2):e3002974. doi: 10.1371/journal.pbio.3002974. eCollection 2025 Feb.
3
Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.

本文引用的文献

1
Disruption of mitochondrial complex I induces progressive parkinsonism.线粒体复合物 I 的破坏会导致进行性帕金森病。
Nature. 2021 Nov;599(7886):650-656. doi: 10.1038/s41586-021-04059-0. Epub 2021 Nov 3.
2
Mitochondrial Dysfunction and Mitophagy in Parkinson's Disease: From Mechanism to Therapy.线粒体功能障碍与帕金森病中的自噬:从机制到治疗。
Trends Biochem Sci. 2021 Apr;46(4):329-343. doi: 10.1016/j.tibs.2020.11.007. Epub 2020 Dec 13.
3
Reversing a model of Parkinson's disease with in situ converted nigral neurons.利用原位转化的黑质神经元逆转帕金森病模型。
中脑多巴胺神经元的慢性过度激活会导致多巴胺神经元优先退化。
bioRxiv. 2025 Mar 4:2024.04.05.588321. doi: 10.1101/2024.04.05.588321.
4
Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson's disease.线粒体靶向二甲双胍通过激活帕金森病细胞培养模型和MitoPark动物模型中的上游蛋白激酶D1(PKD1)信号传导,预防线粒体功能障碍和多巴胺能神经元变性。
Front Neurosci. 2024 Feb 21;18:1356703. doi: 10.3389/fnins.2024.1356703. eCollection 2024.
5
Ionizing radiation-induced mitophagy promotes ferroptosis by increasing intracellular free fatty acids.电离辐射诱导的自噬通过增加细胞内游离脂肪酸促进铁死亡。
Cell Death Differ. 2023 Nov;30(11):2432-2445. doi: 10.1038/s41418-023-01230-0. Epub 2023 Oct 12.
6
HS-based fluorescent imaging for pathophysiological processes.基于HS的病理生理过程荧光成像。
Front Chem. 2023 Jan 27;11:1126309. doi: 10.3389/fchem.2023.1126309. eCollection 2023.
7
Neuroprotective Effects of Sodium Butyrate and Monomethyl Fumarate Treatment through GPR109A Modulation and Intestinal Barrier Restoration on PD Mice.丁酸钠和单甲基富马酸通过 GPR109A 调节和肠道屏障修复对 PD 小鼠的神经保护作用。
Nutrients. 2022 Oct 7;14(19):4163. doi: 10.3390/nu14194163.
8
Insulin-like Growth Factor II Prevents MPP+ and Glucocorticoid Mitochondrial-Oxidative and Neuronal Damage in Dopaminergic Neurons.胰岛素样生长因子II可预防多巴胺能神经元中的1-甲基-4-苯基吡啶离子(MPP+)和糖皮质激素引起的线粒体氧化及神经元损伤。
Antioxidants (Basel). 2021 Dec 24;11(1):41. doi: 10.3390/antiox11010041.
Nature. 2020 Jun;582(7813):550-556. doi: 10.1038/s41586-020-2388-4. Epub 2020 Jun 24.
4
Mitochondrial DNA Depletion in Respiratory Chain-Deficient Parkinson Disease Neurons.呼吸链缺陷型帕金森病神经元中的线粒体DNA耗竭
Ann Neurol. 2016 Mar;79(3):366-78. doi: 10.1002/ana.24571. Epub 2016 Jan 28.
5
Understanding the susceptibility of dopamine neurons to mitochondrial stressors in Parkinson's disease.了解帕金森病中多巴胺能神经元对线粒体应激源的易感性。
FEBS Lett. 2015 Dec 21;589(24 Pt A):3702-13. doi: 10.1016/j.febslet.2015.10.021. Epub 2015 Oct 23.
6
Genetic reduction of mitochondrial complex I function does not lead to loss of dopamine neurons in vivo.线粒体复合体I功能的基因下调在体内不会导致多巴胺能神经元的丧失。
Neurobiol Aging. 2015 Sep;36(9):2617-27. doi: 10.1016/j.neurobiolaging.2015.05.008. Epub 2015 May 16.
7
Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.线粒体功能障碍和帕金森病中的自噬:从家族性到散发性疾病。
Trends Biochem Sci. 2015 Apr;40(4):200-10. doi: 10.1016/j.tibs.2015.02.003. Epub 2015 Mar 8.
8
Loss of mitochondrial fission depletes axonal mitochondria in midbrain dopamine neurons.线粒体分裂功能丧失会耗尽中脑多巴胺能神经元轴突中的线粒体。
J Neurosci. 2014 Oct 22;34(43):14304-17. doi: 10.1523/JNEUROSCI.0930-14.2014.
9
Disease duration and the integrity of the nigrostriatal system in Parkinson's disease.帕金森病的疾病持续时间与黑质纹状体系统的完整性。
Brain. 2013 Aug;136(Pt 8):2419-31. doi: 10.1093/brain/awt192.
10
Altered dopamine metabolism and increased vulnerability to MPTP in mice with partial deficiency of mitochondrial complex I in dopamine neurons.多巴胺神经元中线粒体复合物 I 部分缺乏的小鼠多巴胺代谢改变和对 MPTP 易感性增加。
Hum Mol Genet. 2012 Mar 1;21(5):1078-89. doi: 10.1093/hmg/ddr537. Epub 2011 Nov 16.