• 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

跨物种研究表明,线粒体基因表达失调和电子传递复合物 I 活性的失调对肌肉减少症至关重要。

Cross-Species Studies Reveal That Dysregulated Mitochondrial Gene Expression and Electron Transport Complex I Activity Are Crucial for Sarcopenia.

机构信息

Department of Food Science and Nutrition, Kyungpook National University, 80, Daehak-ro, Buk-Ku, Daegu 41566, Republic of Korea.

Center for Food and Nutritional Genomics Research, Kyungpook National University, 80, Daehak-ro, Buk-Ku, Daegu 41566, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Sep 25;25(19):10302. doi: 10.3390/ijms251910302.

DOI:10.3390/ijms251910302
PMID:39408631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11477305/
Abstract

The significance of complex I of the electron transport chain (ETC) in the aging process is widely acknowledged; however, its specific impact on the development of sarcopenia in muscle remains poorly understood. This study elucidated the correlation between complex I inhibition and sarcopenia by conducting a comparative analysis of skeletal muscle gene expression in sarcopenia phenotypes from rats, mice, and humans. Our findings reveal a common mechanistic link across species, particularly highlighting the correlation between the suppression of complex I of ETC activity and dysregulated mitochondrial transcription and translation in sarcopenia phenotypes. Additionally, we observed macrophage dysfunction alongside abnormal metabolic processes within skeletal muscle tissues across all species, implicating their pathogenic role in the onset of sarcopenia. These discoveries underscore the importance of understanding the shared mechanisms associated with complex I of ETC in sarcopenia development. The identified correlations provide valuable insights into potential targets for therapeutic interventions aimed at mitigating the impact of sarcopenia, a condition with substantial implications for aging populations.

摘要

电子传递链(ETC)复合体 I 在衰老过程中的重要性已被广泛认可;然而,其对肌肉中进行性肌肉减少症发展的具体影响仍知之甚少。本研究通过对大鼠、小鼠和人类进行性肌肉减少症表型的骨骼肌基因表达进行比较分析,阐明了复合体 I 抑制与进行性肌肉减少症之间的相关性。我们的研究结果揭示了物种间存在共同的机制联系,特别是突出了 ETC 活性复合体 I 抑制与进行性肌肉减少症表型中线粒体转录和翻译失调之间的相关性。此外,我们观察到所有物种的骨骼肌组织中存在巨噬细胞功能障碍以及异常代谢过程,表明它们在进行性肌肉减少症的发病机制中具有致病作用。这些发现强调了理解与 ETC 复合体 I 相关的共同机制在进行性肌肉减少症发展中的重要性。所确定的相关性为治疗干预的潜在靶点提供了有价值的见解,这些靶点旨在减轻进行性肌肉减少症的影响,这种情况对老年人口具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/6626570d72a2/ijms-25-10302-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/41cdc20b4194/ijms-25-10302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/b5e072bf3f4b/ijms-25-10302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/20dea1ddb75e/ijms-25-10302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/b1743be91418/ijms-25-10302-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/6626570d72a2/ijms-25-10302-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/41cdc20b4194/ijms-25-10302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/b5e072bf3f4b/ijms-25-10302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/20dea1ddb75e/ijms-25-10302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/b1743be91418/ijms-25-10302-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecea/11477305/6626570d72a2/ijms-25-10302-g005.jpg

相似文献

1
Cross-Species Studies Reveal That Dysregulated Mitochondrial Gene Expression and Electron Transport Complex I Activity Are Crucial for Sarcopenia.跨物种研究表明,线粒体基因表达失调和电子传递复合物 I 活性的失调对肌肉减少症至关重要。
Int J Mol Sci. 2024 Sep 25;25(19):10302. doi: 10.3390/ijms251910302.
2
Loss of high-temperature requirement protein A2 protease activity induces mitonuclear imbalance via differential regulation of mitochondrial biogenesis in sarcopenia.高温需求蛋白 A2 蛋白酶活性丧失通过差异调节线粒体生物发生诱导肌肉减少症中的线粒体-核失衡。
IUBMB Life. 2020 Aug;72(8):1659-1679. doi: 10.1002/iub.2289. Epub 2020 Apr 30.
3
Mitochondrial DNA mutations induce mitochondrial dysfunction, apoptosis and sarcopenia in skeletal muscle of mitochondrial DNA mutator mice.线粒体 DNA 突变导致线粒体 DNA 突变小鼠骨骼肌线粒体功能障碍、细胞凋亡和肌肉减少症。
PLoS One. 2010 Jul 7;5(7):e11468. doi: 10.1371/journal.pone.0011468.
4
Molecular and phenotypic analysis of rodent models reveals conserved and species-specific modulators of human sarcopenia.啮齿动物模型的分子和表型分析揭示了人类肌肉减少症的保守和物种特异性调节因子。
Commun Biol. 2021 Feb 12;4(1):194. doi: 10.1038/s42003-021-01723-z.
5
Denervated muscle fibers induce mitochondrial peroxide generation in neighboring innervated fibers: Role in muscle aging.去神经的肌纤维会诱导邻近神经支配的纤维中线粒体产生过氧化物:在肌肉衰老中的作用。
Free Radic Biol Med. 2017 Nov;112:84-92. doi: 10.1016/j.freeradbiomed.2017.07.017. Epub 2017 Jul 21.
6
Age-dependent increase in angiopoietin-like protein 2 accelerates skeletal muscle loss in mice.年龄依赖性的血管生成素样蛋白 2 增加加速了小鼠的骨骼肌丢失。
J Biol Chem. 2018 Feb 2;293(5):1596-1609. doi: 10.1074/jbc.M117.814996. Epub 2017 Nov 30.
7
Effects of Nrf2 deficiency on mitochondrial oxidative stress in aged skeletal muscle.Nrf2基因缺失对衰老骨骼肌线粒体氧化应激的影响。
Physiol Rep. 2019 Feb;7(3):e13998. doi: 10.14814/phy2.13998.
8
Mesenchymal Bmp3b expression maintains skeletal muscle integrity and decreases in age-related sarcopenia.间充质 Bmp3b 表达维持骨骼肌完整性,并随着年龄相关的肌肉减少症而减少。
J Clin Invest. 2021 Jan 4;131(1). doi: 10.1172/JCI139617.
9
Mitochondrial morphology is altered in atrophied skeletal muscle of aged mice.老年小鼠萎缩骨骼肌中的线粒体形态发生改变。
Oncotarget. 2015 Jul 20;6(20):17923-37. doi: 10.18632/oncotarget.4235.
10
Role of Age-Related Mitochondrial Dysfunction in Sarcopenia.衰老相关的线粒体功能障碍在肌肉减少症中的作用。
Int J Mol Sci. 2020 Jul 23;21(15):5236. doi: 10.3390/ijms21155236.

本文引用的文献

1
D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance.D-阿洛酮糖可改善失调的巨噬细胞功能和线粒体 NADH 稳态,减轻肥胖引起的胰岛素抵抗。
Nutrients. 2023 Sep 29;15(19):4218. doi: 10.3390/nu15194218.
2
Chronic inflammation in high-fat diet-fed mice: Unveiling the early pathogenic connection between liver and adipose tissue.高脂肪饮食喂养的小鼠中的慢性炎症:揭示肝脏和脂肪组织之间早期的致病联系。
J Autoimmun. 2023 Sep;139:103091. doi: 10.1016/j.jaut.2023.103091. Epub 2023 Aug 16.
3
Changes in macrophage immunometabolism as a marker of skeletal muscle dysfunction across the lifespan.
巨噬细胞免疫代谢变化作为贯穿整个生命周期的骨骼肌功能障碍的标志物。
Aging (Albany NY). 2023 May 25;15(10):4035-4050. doi: 10.18632/aging.204750.
4
Mitochondrial Complex I, a Possible Sensible Site of cAMP Pathway in Aging.线粒体复合体I,衰老过程中cAMP信号通路的一个可能敏感位点。
Antioxidants (Basel). 2023 Jan 18;12(2):221. doi: 10.3390/antiox12020221.
5
Immunometabolism of macrophages regulates skeletal muscle regeneration.巨噬细胞的免疫代谢调节骨骼肌再生。
Front Cell Dev Biol. 2022 Sep 6;10:948819. doi: 10.3389/fcell.2022.948819. eCollection 2022.
6
Metabolomic profiles to explore biomarkers of severe sarcopenia in older men: A pilot study.探索老年男性严重肌肉减少症生物标志物的代谢组学特征:一项初步研究。
Exp Gerontol. 2022 Oct 1;167:111924. doi: 10.1016/j.exger.2022.111924. Epub 2022 Aug 10.
7
Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice.线粒体复合物 I 亚基 Ndufs2 的表达减少不会影响小鼠的健康寿命。
Sci Rep. 2022 Mar 25;12(1):5196. doi: 10.1038/s41598-022-09074-3.
8
Molecular Basis for the Therapeutic Effects of Exercise on Mitochondrial Defects.运动对线粒体缺陷治疗作用的分子基础
Front Physiol. 2021 Jan 13;11:615038. doi: 10.3389/fphys.2020.615038. eCollection 2020.
9
Mitochondrial Impairment in Sarcopenia.肌肉减少症中的线粒体损伤
Biology (Basel). 2021 Jan 6;10(1):31. doi: 10.3390/biology10010031.
10
Age-related decline of interferon-gamma responses in macrophage impairs satellite cell proliferation and regeneration.年龄相关的巨噬细胞干扰素-γ反应下降会损害卫星细胞的增殖和再生。
J Cachexia Sarcopenia Muscle. 2020 Oct;11(5):1291-1305. doi: 10.1002/jcsm.12584. Epub 2020 Jul 29.