• 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

内质网-线粒体相互作用:动脉粥样硬化发展的新机制

Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.

作者信息

Li Mingxiao, Xiao Yili, Dai Ling, Chen Simin, Pei Wanjuan, Tan Chao

机构信息

Medical School, Hunan University of Chinese Medicine, Changsha, China.

Department of Cardiology, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.

出版信息

Front Endocrinol (Lausanne). 2025 Jun 5;16:1573499. doi: 10.3389/fendo.2025.1573499. eCollection 2025.

DOI:10.3389/fendo.2025.1573499
PMID:40538812
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12176567/
Abstract

Atherosclerosis (AS) is a global public health concern and involves a complex pathogenesis characterized by lipid abnormalities, oxidative stress, and inflammatory responses at the cellular and molecular levels. The crosstalk between the endoplasmic reticulum (ER) and mitochondria, mediated by mitochondria-associated membranes (MAMs), plays a critical role in the pathogenesis of atherosclerosis. As two key cellular organelles, the ER and mitochondria interact physically and functionally through MAMs, which serve as bridges between their close contact and interdependence. MAMs maintain lipid homeostasis, promote calcium ion transport, the oxidative stress response, apoptosis, and autophagy. Recent studies have highlighted the significance of ER-mitochondria crosstalk in the progression of AS, as indicated by mitochondrial and ER structural and functional integrity, redox homeostasis, and calcium homeostasis. This review comprehensively explores the novel mechanisms of ER-mitochondria crosstalk in AS and emphasizes the potential of MAMs as therapeutic targets, aiming to provide new perspectives and strategies for the treatment of cardiovascular diseases.

摘要

动脉粥样硬化(AS)是一个全球性的公共卫生问题,其发病机制复杂,在细胞和分子水平上具有脂质异常、氧化应激和炎症反应等特征。由线粒体相关膜(MAM)介导的内质网(ER)与线粒体之间的相互作用在动脉粥样硬化的发病机制中起关键作用。作为两个关键的细胞器,内质网和线粒体通过线粒体相关膜在物理和功能上相互作用,线粒体相关膜充当它们紧密接触和相互依存之间的桥梁。线粒体相关膜维持脂质稳态,促进钙离子运输、氧化应激反应、细胞凋亡和自噬。最近的研究强调了内质网-线粒体相互作用在动脉粥样硬化进展中的重要性,线粒体和内质网的结构和功能完整性、氧化还原稳态和钙稳态都表明了这一点。这篇综述全面探讨了内质网-线粒体相互作用在动脉粥样硬化中的新机制,并强调了线粒体相关膜作为治疗靶点的潜力,旨在为心血管疾病的治疗提供新的视角和策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/58b4d800cc1b/fendo-16-1573499-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/7fcf6949052b/fendo-16-1573499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/2292710ef01d/fendo-16-1573499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/58b4d800cc1b/fendo-16-1573499-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/7fcf6949052b/fendo-16-1573499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/2292710ef01d/fendo-16-1573499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3d0/12176567/58b4d800cc1b/fendo-16-1573499-g003.jpg

相似文献

1
Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.内质网-线粒体相互作用:动脉粥样硬化发展的新机制
Front Endocrinol (Lausanne). 2025 Jun 5;16:1573499. doi: 10.3389/fendo.2025.1573499. eCollection 2025.
2
Dendrobine attenuates lipopolysaccharide-induced acute lung injury by modulating FAM134B-mediated endoplasmic reticulum autophagy and mitochondrial function.石蒜碱通过调节FAM134B介导的内质网自噬和线粒体功能减轻脂多糖诱导的急性肺损伤。
Phytomedicine. 2025 Aug;144:156952. doi: 10.1016/j.phymed.2025.156952. Epub 2025 Jun 5.
3
GRINA alleviates hepatic ischemia‒reperfusion injury-induced apoptosis and ER-phagy by enhancing HRD1-mediated ATF6 ubiquitination.GRINA通过增强HRD1介导的ATF6泛素化来减轻肝缺血再灌注损伤诱导的细胞凋亡和内质网自噬。
J Hepatol. 2025 Jan 22. doi: 10.1016/j.jhep.2025.01.012.
4
Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis.微蛋白作为内质网功能和细胞稳态的关键调节因子的新作用。
Semin Cell Dev Biol. 2025 Jun;170:103608. doi: 10.1016/j.semcdb.2025.103608. Epub 2025 Apr 17.
5
Unfolded protein response in endoplasmic reticulum stress associated with retinal degenerative diseases: A promising therapeutic target.内质网应激中与视网膜退行性疾病相关的未折叠蛋白反应:一个有前景的治疗靶点。
Neural Regen Res. 2025 Jun 19. doi: 10.4103/NRR.NRR-D-24-01124.
6
Hyperoxia-induced senescence in fetal airway smooth muscle cells: role of mitochondrial reactive oxygen species and endoplasmic reticulum stress.高氧诱导胎儿气道平滑肌细胞衰老:线粒体活性氧和内质网应激的作用
Am J Physiol Lung Cell Mol Physiol. 2025 Jul 1;329(1):L1-L18. doi: 10.1152/ajplung.00348.2024. Epub 2025 Apr 4.
7
Transient receptor potential vanilloid channel 2 contributes to multi-modal endoplasmic reticulum and perinuclear space dilations that can also be observed in prion-infected mice.瞬时受体电位香草酸亚型通道2会导致多模式内质网和核周间隙扩张,这种扩张在朊病毒感染的小鼠中也能观察到。
Acta Neuropathol. 2025 Jun 23;149(1):68. doi: 10.1007/s00401-025-02906-2.
8
Exploring Triptolide's Dual Role in Inflammation and Oxidative Stress: Responses of Organelles.探索雷公藤甲素在炎症和氧化应激中的双重作用:细胞器的反应
J Biochem Mol Toxicol. 2025 Jul;39(7):e70371. doi: 10.1002/jbt.70371.
9
Mitochondria and Endoplasmic Reticulum Contact Site as a Regulator of Proteostatic Stress Responses in Neurodegenerative Diseases.线粒体与内质网接触位点作为神经退行性疾病中蛋白质稳态应激反应的调节因子
Bioessays. 2025 May 4:e70016. doi: 10.1002/bies.70016.
10
Adenovirus Modulates Toll-Like Receptor 4 Signaling by Reprogramming ORP1L-VAP Protein Contacts for Cholesterol Transport from Endosomes to the Endoplasmic Reticulum.腺病毒通过重新编程ORP1L-VAP蛋白接触点来调节Toll样受体4信号通路,以实现胆固醇从内体到内质网的转运。
J Virol. 2017 Feb 28;91(6). doi: 10.1128/JVI.01904-16. Print 2017 Mar 15.

本文引用的文献

1
Mitochondrial DNA in atherosclerosis: Mechanisms, biomarker potential, and therapeutic perspectives.动脉粥样硬化中的线粒体DNA:机制、生物标志物潜力及治疗前景
Int Immunopharmacol. 2025 Apr 16;152:114449. doi: 10.1016/j.intimp.2025.114449. Epub 2025 Mar 11.
2
New insights into the relationship of mitochondrial metabolism and atherosclerosis.线粒体代谢与动脉粥样硬化关系的新见解。
Cell Signal. 2025 Mar;127:111580. doi: 10.1016/j.cellsig.2024.111580. Epub 2024 Dec 26.
3
Statins Combined with AAV8-TBG-LOX-1 Reduce the Vascular Lipid-driven Inflammatory Response and Inhibit Atherosclerosis.
他汀类药物联合腺相关病毒8型-甲状腺素结合球蛋白-凝集素样氧化低密度脂蛋白受体1可减轻血管脂质驱动的炎症反应并抑制动脉粥样硬化。
Curr Med Sci. 2024 Dec;44(6):1097-1102. doi: 10.1007/s11596-024-2954-3. Epub 2024 Dec 4.
4
Ferulic acid and protocatechuic acid alleviate atherosclerosis by promoting UCP1 expression to inhibit the NLRP3-IL-1β signaling pathway.阿魏酸和原儿茶酸通过促进解偶联蛋白1(UCP1)表达以抑制NLRP3-白细胞介素-1β(IL-1β)信号通路来减轻动脉粥样硬化。
Food Funct. 2025 Jan 2;16(1):40-53. doi: 10.1039/d4fo02955k.
5
The augment effects of magnesium hydride on the lipid lowering effect of atorvastatin: an in vivo and in vitro investigation.研究探讨了氢化镁对阿托伐他汀降血脂作用的增强效果:体内和体外研究。
Med Gas Res. 2025 Mar 1;15(1):148-155. doi: 10.4103/mgr.MEDGASRES-D-23-00047. Epub 2024 Jul 25.
6
Attenuation of PM2.5-Induced Lung Injury by 4-Phenylbutyric Acid: Maintenance of [Ca]i Stability between Endoplasmic Reticulum and Mitochondria.4- 苯基丁酸减轻 PM2.5 诱导的肺损伤:内质网和线粒体之间 [Ca]i 稳定性的维持。
Biomolecules. 2024 Sep 8;14(9):1135. doi: 10.3390/biom14091135.
7
Corrigendum: Effect of a high dose atorvastatin as added-on therapy on symptoms and serum AMPK/NLRP3 inflammasome and IL-6/STAT3 axes in patients with major depressive disorder: randomized controlled clinical study.勘误:高剂量阿托伐他汀作为附加治疗对重度抑郁症患者症状及血清AMPK/NLRP3炎性小体和IL-6/STAT3信号轴的影响:随机对照临床研究。
Front Pharmacol. 2024 Aug 29;15:1464358. doi: 10.3389/fphar.2024.1464358. eCollection 2024.
8
Mitochondria-endoplasmic reticulum crosstalk in apoptosis: The interactions of cytochrome c with monooxygenase and its reductase.线粒体-内质网在细胞凋亡中的相互作用:细胞色素 c 与单加氧酶及其还原酶的相互作用。
Int J Biol Macromol. 2024 Nov;279(Pt 1):135160. doi: 10.1016/j.ijbiomac.2024.135160. Epub 2024 Aug 29.
9
Augmented microglial endoplasmic reticulum-mitochondria contacts mediate depression-like behavior in mice induced by chronic social defeat stress.慢性社会挫败应激诱导的小鼠抑郁样行为中增强的小胶质细胞内质网-线粒体接触。
Nat Commun. 2024 Jun 18;15(1):5199. doi: 10.1038/s41467-024-49597-z.
10
Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases.线粒体相关内质网膜作为心血管疾病的治疗靶点
Front Pharmacol. 2024 Apr 17;15:1398381. doi: 10.3389/fphar.2024.1398381. eCollection 2024.