• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

代谢功能障碍与多发性硬化症中的过氧化物酶体增殖物激活受体(PPAR)

Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis.

机构信息

Centro de Investigação Interdisciplinar Egas Moniz (CiiEM), Instituto Universitário Egas Moniz, Campus Universitário, Quinta da Granja, Monte de Caparica, 2819-511 Caparica, Portugal.

Centro Hospitalar de Lisboa Central, EPE, Hospital de Santo António dos Capuchos, Departamento de Neurociências, Alameda de Santo António dos Capuchos, 1169-050 Lisboa, Portugal.

出版信息

Int J Mol Sci. 2018 Jun 1;19(6):1639. doi: 10.3390/ijms19061639.

DOI:10.3390/ijms19061639
PMID:29865151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6032172/
Abstract

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system (CNS) probably caused, in most cases, by the interaction of genetic and environmental factors. This review first summarizes some clinical, epidemiological and pathological characteristics of MS. Then, the involvement of biochemical pathways is discussed in the development and repair of the CNS lesions and the immune dysfunction in the disease. Finally, the potential roles of peroxisome proliferator-activated receptors (PPAR) in MS are discussed. It is suggested that metabolic mechanisms modulated by PPAR provide a window to integrate the systemic and neurological events underlying the pathogenesis of the disease. In conclusion, the reviewed data highlight molecular avenues of understanding MS that may open new targets for improved therapies and preventive strategies for the disease.

摘要

多发性硬化症(MS)是一种中枢神经系统(CNS)的炎症性和神经退行性疾病,可能由遗传和环境因素相互作用引起。本文首先总结了 MS 的一些临床、流行病学和病理学特征。然后,讨论了生化途径在 CNS 损伤的发展和修复以及疾病中的免疫功能障碍中的作用。最后,讨论了过氧化物酶体增殖物激活受体(PPAR)在 MS 中的潜在作用。研究表明,PPAR 调节的代谢机制为整合疾病发病机制中涉及的全身和神经事件提供了一个窗口。总之,综述的数据突出了理解 MS 的分子途径,这些途径可能为该疾病的治疗和预防策略提供新的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eed/6032172/4a824f2a1a92/ijms-19-01639-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eed/6032172/4a824f2a1a92/ijms-19-01639-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eed/6032172/4a824f2a1a92/ijms-19-01639-g001.jpg

相似文献

1
Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis.代谢功能障碍与多发性硬化症中的过氧化物酶体增殖物激活受体(PPAR)
Int J Mol Sci. 2018 Jun 1;19(6):1639. doi: 10.3390/ijms19061639.
2
Exploiting the Therapeutic Potential of Endogenous Immunomodulatory Systems in Multiple Sclerosis-Special Focus on the Peroxisome Proliferator-Activated Receptors (PPARs) and the Kynurenines.挖掘多发性硬化症中内源性免疫调节系统的治疗潜力——特别关注过氧化物酶体增殖物激活受体 (PPARs) 和犬尿氨酸。
Int J Mol Sci. 2019 Jan 19;20(2):426. doi: 10.3390/ijms20020426.
3
Peroxisome proliferator-activated receptor (PPAR)β/δ, a possible nexus of PPARα- and PPARγ-dependent molecular pathways in neurodegenerative diseases: Review and novel hypotheses.过氧化物酶体增殖物激活受体 (PPAR)β/δ,神经退行性疾病中 PPARα 和 PPARγ 依赖的分子途径的可能连接点:综述和新假说。
Neurochem Int. 2013 Oct;63(4):322-30. doi: 10.1016/j.neuint.2013.06.012. Epub 2013 Jun 25.
4
Unlike PPARgamma, neither other PPARs nor PGC-1alpha is elevated in the cerebrospinal fluid of patients with multiple sclerosis.与过氧化物酶体增殖物激活受体γ(PPARγ)不同,多发性硬化症患者脑脊液中的其他过氧化物酶体增殖物激活受体(PPARs)和过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1α)均未升高。
Neurosci Lett. 2017 Jun 9;651:128-133. doi: 10.1016/j.neulet.2017.05.008. Epub 2017 May 5.
5
Multiple sclerosis is not a disease of the immune system.多发性硬化症不是免疫系统疾病。
Q Rev Biol. 2011 Dec;86(4):287-321. doi: 10.1086/662453.
6
Peroxisome proliferator-activated receptor agonist regulation of glial activation: relevance to CNS inflammatory disorders.过氧化物酶体增殖物激活受体激动剂对神经胶质细胞激活的调节:与中枢神经系统炎症性疾病的相关性
Neurochem Int. 2006 Jul;49(2):183-9. doi: 10.1016/j.neuint.2006.04.003. Epub 2006 Jun 5.
7
Peroxisome proliferator-activated receptors (PPARs) as therapeutic target in neurodegenerative disorders.过氧化物酶体增殖物激活受体(PPARs)作为神经退行性疾病的治疗靶点。
Biochem Biophys Res Commun. 2017 Feb 19;483(4):1166-1177. doi: 10.1016/j.bbrc.2016.08.043. Epub 2016 Aug 8.
8
PPARs in the central nervous system: roles in neurodegeneration and neuroinflammation.中枢神经系统中的过氧化物酶体增殖物激活受体:在神经退行性变和神经炎症中的作用。
Biol Rev Camb Philos Soc. 2017 Nov;92(4):2046-2069. doi: 10.1111/brv.12320. Epub 2017 Feb 20.
9
Peroxisome proliferator-activated receptors as transcriptional nodal points and therapeutic targets.过氧化物酶体增殖物激活受体作为转录节点和治疗靶点。
Circulation. 2007 Jan 30;115(4):518-33. doi: 10.1161/CIRCULATIONAHA.104.475673.
10
The roles of peroxisome proliferator-activated receptors in the metabolic syndrome.过氧化物酶体增殖物激活受体在代谢综合征中的作用。
Prog Mol Biol Transl Sci. 2014;121:217-66. doi: 10.1016/B978-0-12-800101-1.00007-7.

引用本文的文献

1
Peroxisomes as emerging clinical targets in neuroinflammatory diseases.过氧化物酶体作为神经炎症性疾病中新兴的临床靶点。
Front Mol Neurosci. 2025 Aug 29;18:1642590. doi: 10.3389/fnmol.2025.1642590. eCollection 2025.
2
Retinoid X Receptor as a Therapeutic Target to Treat Neurological Disorders Associated with α-Synucleinopathy.视黄酸X受体作为治疗与α-突触核蛋白病相关神经疾病的治疗靶点。
Cells. 2025 May 9;14(10):685. doi: 10.3390/cells14100685.
3
VCAM-1 Mesenchymal Stem/Stromal Cells Reveal Preferable Efficacy Upon an Experimental Autoimmune Encephalomyelitis Mouse Model of Multiple Sclerosis Over the VCAM-1 Counterpart.

本文引用的文献

1
Early alpha-lipoic acid therapy protects from degeneration of the inner retinal layers and vision loss in an experimental autoimmune encephalomyelitis-optic neuritis model.早期硫辛酸治疗可预防实验性自身免疫性脑脊髓炎-视神经炎模型中内视网膜层的退化和视力丧失。
J Neuroinflammation. 2018 Mar 7;15(1):71. doi: 10.1186/s12974-018-1111-y.
2
Multiple Sclerosis: Mechanisms and Immunotherapy.多发性硬化症:机制与免疫疗法。
Neuron. 2018 Feb 21;97(4):742-768. doi: 10.1016/j.neuron.2018.01.021.
3
The Role of Lipid Metabolism in T Lymphocyte Differentiation and Survival.
VCAM-1 间充质干细胞/基质细胞在实验性自身免疫性脑脊髓炎多发性硬化症小鼠模型中比 VCAM-1 对照物显示出更好的疗效。
Neurochem Res. 2024 Nov 30;50(1):40. doi: 10.1007/s11064-024-04267-w.
4
Defective Integrator activity shapes the transcriptome of patients with multiple sclerosis.缺陷整合酶活性塑造多发性硬化症患者的转录组。
Life Sci Alliance. 2024 Jul 19;7(10). doi: 10.26508/lsa.202402586. Print 2024 Oct.
5
Cellular and Molecular Evidence of Multiple Sclerosis Diagnosis and Treatment Challenges.多发性硬化症诊断与治疗挑战的细胞和分子证据
J Clin Med. 2023 Jun 26;12(13):4274. doi: 10.3390/jcm12134274.
6
Fingolimod treatment modulates PPARγ and CD36 gene expression in women with multiple sclerosis.芬戈莫德治疗可调节多发性硬化症女性患者的PPARγ和CD36基因表达。
Front Mol Neurosci. 2022 Dec 15;15:1077381. doi: 10.3389/fnmol.2022.1077381. eCollection 2022.
7
Fingolimod effects on the brain are mediated through biochemical modulation of bioenergetics, autophagy, and neuroinflammatory networks.芬戈莫德对大脑的作用是通过对生物能量学、自噬和神经炎症网络的生化调节来介导的。
Proteomics. 2022 Oct;22(19-20):e2100247. doi: 10.1002/pmic.202100247. Epub 2022 Aug 8.
8
Role of Phytoconstituents as PPAR Agonists: Implications for Neurodegenerative Disorders.植物成分作为过氧化物酶体增殖物激活受体激动剂的作用:对神经退行性疾病的影响。
Biomedicines. 2021 Dec 14;9(12):1914. doi: 10.3390/biomedicines9121914.
9
Targeting white matter neuroprotection as a relapse prevention strategy for treatment of cocaine use disorder: Design of a mechanism-focused randomized clinical trial.以白质神经保护为靶点,预防可卡因使用障碍复发的治疗策略:一项以机制为重点的随机临床试验设计。
Contemp Clin Trials. 2021 Dec;111:106603. doi: 10.1016/j.cct.2021.106603. Epub 2021 Oct 22.
10
Repurposing Peroxisome Proliferator-Activated Receptor Agonists in Neurological and Psychiatric Disorders.在神经和精神疾病中重新利用过氧化物酶体增殖物激活受体激动剂。
Pharmaceuticals (Basel). 2021 Oct 8;14(10):1025. doi: 10.3390/ph14101025.
脂质代谢在T淋巴细胞分化和存活中的作用。
Front Immunol. 2018 Jan 12;8:1949. doi: 10.3389/fimmu.2017.01949. eCollection 2017.
4
Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response.膳食盐通过肠道起始的 TH17 反应促进神经血管和认知功能障碍。
Nat Neurosci. 2018 Feb;21(2):240-249. doi: 10.1038/s41593-017-0059-z. Epub 2018 Jan 15.
5
Multiple Sclerosis.多发性硬化症
N Engl J Med. 2018 Jan 11;378(2):169-180. doi: 10.1056/NEJMra1401483.
6
An introduction to the microbiome and MS.肠道微生物组与多发性硬化症简介。
Mult Scler. 2018 Jan;24(1):53-57. doi: 10.1177/1352458517737391.
7
Dietary fatty acids and susceptibility to multiple sclerosis.膳食脂肪酸与多发性硬化症易感性。
Mult Scler. 2018 Jan;24(1):12-16. doi: 10.1177/1352458517737372.
8
Cell-specific and region-specific transcriptomics in the multiple sclerosis model: Focus on astrocytes.多发性硬化症模型中的细胞特异性和区域特异性转录组学:关注星形胶质细胞。
Proc Natl Acad Sci U S A. 2018 Jan 9;115(2):E302-E309. doi: 10.1073/pnas.1716032115. Epub 2017 Dec 26.
9
Low-Density Lipoprotein Receptor Deficiency Attenuates Neuroinflammation through the Induction of Apolipoprotein E.低密度脂蛋白受体缺陷通过诱导载脂蛋白E减轻神经炎症。
Front Immunol. 2017 Nov 30;8:1701. doi: 10.3389/fimmu.2017.01701. eCollection 2017.
10
Machine learning shows association between genetic variability in and cerebral connectivity in preterm infants.机器学习显示了 与早产儿大脑连接之间的遗传变异性之间的关联。
Proc Natl Acad Sci U S A. 2017 Dec 26;114(52):13744-13749. doi: 10.1073/pnas.1704907114. Epub 2017 Dec 11.