Mitochondrial dysfunction as a critical event in the pathophysiology of bipolar disorder.

Mitochondrial dysfunction as a critical event in the pathophysiology of bipolar disorder.
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线粒体功能障碍是双相情感障碍病理生理学中的一个关键事件。

DOI:
10.1016/j.mito.2020.12.002
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发表时间:
2021-03
期刊:
影响因子:
4.4
通讯作者:
Quevedo, Joao
Quevedo, Joao
中科院分区:
生物学3区
文献类型:
--
作者:
Scaini, Giselli;Andrews, Taylor;Lima, Camila N. C.;Benevenuto, Deborah;Streck, Emilio L.;Quevedo, Joao

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相似文献

尽管神经生物学研究近期取得了进展,但对双相情感障碍(BD)病理生理学的了解仍然有限。双相情感障碍的线粒体功能障碍假说已得到多项研究的证实,这些研究包括对啮齿动物模型和人类的死后大脑分析、神经影像学以及特定生物标志物的研究。有证据表明,双相情感障碍可能与线粒体形态和动力学异常、神经免疫功能障碍以及非典型的线粒体代谢和氧化应激途径有关。情绪障碍中的线粒体功能障碍还与钙离子水平异常、谷氨酸兴奋性毒性、促凋亡蛋白和抗凋亡蛋白之间向凋亡方向的失衡、电子传递链复合物的基因表达异常以及三磷酸腺苷(ATP)合成减少有关。本文旨在综述和讨论线粒体功能障碍在双相情感障碍病因学中的影响,并探索线粒体作为新型治疗药物的潜在靶点。
The understanding of the pathophysiology of bipolar disorder (BD) remains modest, despite recent advances in neurobiological research. The mitochondrial dysfunction hypothesis of bipolar disorder has been corroborated by several studies involving postmortem brain analysis, neuroimaging, and specific biomarkers in both rodent models and humans. Evidence suggests that BD might be related to abnormal mitochondrial morphology and dynamics, neuroimmune dysfunction, and atypical mitochondrial metabolism and oxidative stress pathways. Mitochondrial dysfunction in mood disorders is also associated with abnormal Ca2+ levels, glutamate excitotoxicity, an imbalance between pro- and antiapoptotic proteins towards apoptosis, abnormal gene expression of electron transport chain complexes, and decreased ATP synthesis. This paper aims to review and discuss the implications of mitochondrial dysfunction in BD etiology and to explore mitochondria as a potential target for novel therapeutic agents.
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