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[Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases].[视神经萎缩1介导的线粒体动力学在骨骼系统疾病中的研究进展]
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2023 Jun 15;37(6):758-763. doi: 10.7507/1002-1892.202302056.
2
OPA1 regulation of mitochondrial dynamics in skeletal and cardiac muscle.OPA1 调节骨骼肌和心肌中的线粒体动态。
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Mitochondrial disorder with OPA1 mutation lacking optic atrophy.伴有OPA1突变但无视神经萎缩的线粒体疾病。
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5
Defective mitochondrial adenosine triphosphate production in skeletal muscle from patients with dominant optic atrophy due to OPA1 mutations.由于OPA1基因突变导致的显性视神经萎缩患者骨骼肌中线粒体三磷酸腺苷生成缺陷。
Arch Neurol. 2011 Jan;68(1):67-73. doi: 10.1001/archneurol.2010.228. Epub 2010 Sep 13.
6
Oxidative insults disrupt OPA1-mediated mitochondrial dynamics in cultured mammalian cells.氧化应激破坏培养的哺乳动物细胞中线粒体解偶联蛋白 1 介导的线粒体动力学。
Redox Rep. 2018 Dec;23(1):160-167. doi: 10.1080/13510002.2018.1492766.
7
Dominant optic atrophy, OPA1, and mitochondrial quality control: understanding mitochondrial network dynamics.优势型视神经萎缩、OPA1 和线粒体质量控制:理解线粒体网络动态。
Mol Neurodegener. 2013 Sep 25;8:32. doi: 10.1186/1750-1326-8-32.
8
TNFR2 Stimulation Promotes Mitochondrial Fusion via Stat3- and NF-kB-Dependent Activation of OPA1 Expression.肿瘤坏死因子受体2(TNFR2)刺激通过Stat3和NF-κB依赖性激活OPA1表达促进线粒体融合。
Circ Res. 2017 Aug 4;121(4):392-410. doi: 10.1161/CIRCRESAHA.117.311143. Epub 2017 Jun 21.
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Not only dominant, not only optic atrophy: expanding the clinical spectrum associated with OPA1 mutations.不仅是显性,不仅是视神经萎缩:扩展与OPA1突变相关的临床谱。
Orphanet J Rare Dis. 2017 May 12;12(1):89. doi: 10.1186/s13023-017-0641-1.
10
The short variant of the mitochondrial dynamin OPA1 maintains mitochondrial energetics and cristae structure.线粒体动力蛋白OPA1的短变体维持线粒体能量代谢和嵴结构。
J Biol Chem. 2017 Apr 28;292(17):7115-7130. doi: 10.1074/jbc.M116.762567. Epub 2017 Mar 15.

本文引用的文献

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Endoplasmic reticulum stress mediated by ROS participates in cadmium exposure-induced MC3T3-E1 cell apoptosis.活性氧介导的内质网应激参与镉暴露诱导的 MC3T3-E1 细胞凋亡。
Ecotoxicol Environ Saf. 2023 Feb;251:114517. doi: 10.1016/j.ecoenv.2023.114517. Epub 2023 Jan 18.
2
The role of the sirtuin family in cartilage and osteoarthritis: molecular mechanisms and therapeutic targets.Sirtuin 家族在软骨和骨关节炎中的作用:分子机制和治疗靶点。
Arthritis Res Ther. 2022 Dec 31;24(1):286. doi: 10.1186/s13075-022-02983-8.
3
supports mitochondrial dynamics and immune evasion to CD8 T cell in lung adenocarcinoma.支持肺腺癌中 CD8 T 细胞的线粒体动力学和免疫逃逸。
PeerJ. 2022 Dec 21;10:e14543. doi: 10.7717/peerj.14543. eCollection 2022.
4
Nanocatalytic Biofunctional MOF Coating on Titanium Implants Promotes Osteoporotic Bone Regeneration through Cooperative Pro-osteoblastogenesis MSC Reprogramming.纳米催化生物功能 MOF 涂层钛植入物通过协同促进成骨前体细胞重编程促进骨质疏松性骨再生。
ACS Nano. 2022 Sep 27;16(9):15397-15412. doi: 10.1021/acsnano.2c07200. Epub 2022 Sep 15.
5
Insight into the interplay between mitochondria-regulated cell death and energetic metabolism in osteosarcoma.骨肉瘤中线粒体调节的细胞死亡与能量代谢之间相互作用的研究进展
Front Cell Dev Biol. 2022 Aug 22;10:948097. doi: 10.3389/fcell.2022.948097. eCollection 2022.
6
Mitochondria Targeted Antioxidant Significantly Alleviates Preeclampsia Caused by 11β-HSD2 Dysfunction via OPA1 and MtDNA Maintenance.线粒体靶向抗氧化剂通过OPA1和线粒体DNA维持显著减轻由11β-羟类固醇脱氢酶2功能障碍引起的子痫前期。
Antioxidants (Basel). 2022 Jul 31;11(8):1505. doi: 10.3390/antiox11081505.
7
Mitochondrial DNA homeostasis impairment and dopaminergic dysfunction: A trembling balance.线粒体DNA稳态受损与多巴胺能功能障碍:一种微妙的平衡。
Ageing Res Rev. 2022 Apr;76:101578. doi: 10.1016/j.arr.2022.101578. Epub 2022 Jan 31.
8
Mitochondrial quality control in cartilage damage and osteoarthritis: new insights and potential therapeutic targets.软骨损伤与骨关节炎中的线粒体质量控制:新见解与潜在治疗靶点
Osteoarthritis Cartilage. 2022 Mar;30(3):395-405. doi: 10.1016/j.joca.2021.10.009. Epub 2021 Oct 29.
9
Cellular senescence in knee osteoarthritis: molecular mechanisms and therapeutic implications.膝骨关节炎中的细胞衰老:分子机制与治疗意义。
Ageing Res Rev. 2021 Sep;70:101413. doi: 10.1016/j.arr.2021.101413. Epub 2021 Jul 21.
10
Moderate mechanical stress suppresses the IL-1β-induced chondrocyte apoptosis by regulating mitochondrial dynamics.适度机械应力通过调节线粒体动力学抑制 IL-1β 诱导的软骨细胞凋亡。
J Cell Physiol. 2021 Nov;236(11):7504-7515. doi: 10.1002/jcp.30386. Epub 2021 Apr 6.

[视神经萎缩1介导的线粒体动力学在骨骼系统疾病中的研究进展]

[Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases].

作者信息

Sun Kaibo, Wu Yuangang, Zeng Yi, Li Mingyang, Wu Limin, Shen Bin

机构信息

Department of Orthopedics, Orthopedic Research Institute, West China Hospital, Sichuan University, Chengdu Sichuan, 610041, P. R. China.

出版信息

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2023 Jun 15;37(6):758-763. doi: 10.7507/1002-1892.202302056.

DOI:10.7507/1002-1892.202302056
PMID:37331956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10277243/
Abstract

OBJECTIVE

To review the research progress of mitochondrial dynamics mediated by optic atrophy 1 (OPA1) in skeletal system diseases.

METHODS

The literatures about OPA1-mediated mitochondrial dynamics in recent years were reviewed, and the bioactive ingredients and drugs for the treatment of skeletal system diseases were summarized, which provided a new idea for the treatment of osteoarthritis.

RESULTS

OPA1 is a key factor involved in mitochondrial dynamics and energetics and in maintaining the stability of the mitochondrial genome. Accumulating evidence indicates that OPA1-mediated mitochondrial dynamics plays an important role in the regulation of skeletal system diseases such as osteoarthritis, osteoporosis, and osteosarcoma.

CONCLUSION

OPA1-mediated mitochondrial dynamics provides an important theoretical basis for the prevention and treatment of skeletal system diseases.

摘要

目的

综述视神经萎缩蛋白1(OPA1)介导的线粒体动力学在骨骼系统疾病中的研究进展。

方法

回顾近年来关于OPA1介导的线粒体动力学的文献,总结治疗骨骼系统疾病的生物活性成分和药物,为骨关节炎的治疗提供新思路。

结果

OPA1是参与线粒体动力学和能量代谢以及维持线粒体基因组稳定性的关键因素。越来越多的证据表明,OPA1介导的线粒体动力学在骨关节炎、骨质疏松症和骨肉瘤等骨骼系统疾病的调控中发挥重要作用。

结论

OPA1介导的线粒体动力学为骨骼系统疾病的防治提供了重要的理论依据。