文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

lnc-MRGPRF-6:1 通过抑制 GPX4 促进 ox-LDL 诱导的巨噬细胞铁死亡。

lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4.

机构信息

Department of Cardiology, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, China.

Department of Geriatrics, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Mediators Inflamm. 2023 Aug 16;2023:5513245. doi: 10.1155/2023/5513245. eCollection 2023.

DOI:10.1155/2023/5513245
PMID:37621767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10447047/
Abstract

BACKGROUND: Ferroptosis, a newly discovered mode of cell death, emerges as a new target for atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are involved in the regulation of ferroptosis. In our previous study, lnc-MRGPRF-6:1 was highly expressed in patients with coronary atherosclerotic disease (CAD) and closely associated with macrophage-mediated inflammation in AS. In the present study, we aim to investigate the role of lnc-MRGPRF-6:1 in oxidized-low-density lipoprotein (ox-LDL)-induced macrophage ferroptosis in AS. METHODS: Firstly, ox-LDL-treated macrophages were used to simulate macrophage injury in AS. Then, ferroptosis-related biomarkers and mitochondrial morphology were detected and observed in ox-LDL-treated macrophages. Subsequently, we constructed lnc-MRGPRF-6:1 knockdown and overexpression of THP-1-derived macrophages and investigated the role of lnc-MRGPRF-6:1 in ox-LDL-induced ferroptosis. Then human monocytes were isolated successfully and were used to explore the role of lnc-MRGPRF-6:1 in macrophage ferroptosis. Likely, we constructed lnc-MRGPRF-6:1 knockdown and overexpression of human monocyte-derived macrophages and detected the expression levels of ferroptosis-related biomarkers. Then, transcriptome sequencing, literature searching, and following quantitative real-time polymerase chain reaction and western blot were implemented to explore specific signaling pathway in the process. It was demonstrated that lnc-MRGPRF-6:1 may regulate ox-LDL-induced macrophage ferroptosis through glutathione peroxidase 4 (GPX4). Eventually, the correlation between lnc-MRGPRF-6:1 and GPX4 was measured in monocyte-derived macrophages of CAD patients and controls. RESULTS: The ox-LDL-induced injury in macrophages was involved in ferroptosis. The knockdown of lnc-MRGPRF-6:1 could alleviate ox-LDL-induced ferroptosis in macrophages. Meanwhile, the overexpression of lnc-MRGPRF-6:1 could intensify ox-LDL-induced ferroptosis. Furthermore, the knockdown of lnc-MRGPRF-6:1 could alleviate the decrease of GPX4 induced by RAS-selective lethal compounds 3 (RSL-3). These indicated that lnc-MRGPRF-6:1 may suppress GPX4 to induce macrophage ferroptosis. Eventually, lnc-MRGPRF-6:1 was highly expressed in the monocyte-derived macrophages of CAD patients and was negatively correlated with the expression of GPX4. CONCLUSION: lnc-MRGPRF-6:1 can promote ox-LDL-induced macrophage ferroptosis through inhibiting GPX4.

摘要

背景：铁死亡是一种新发现的细胞死亡方式，它成为动脉粥样硬化（AS）的新靶点。长链非编码 RNA（lncRNA）参与铁死亡的调控。在我们之前的研究中，lnc-MRGPRF-6：1 在冠心病（CAD）患者中高表达，并与 AS 中巨噬细胞介导的炎症密切相关。本研究旨在探讨 lnc-MRGPRF-6：1 在氧化低密度脂蛋白（ox-LDL）诱导的 AS 巨噬细胞铁死亡中的作用。

方法：首先，用 ox-LDL 处理巨噬细胞模拟 AS 中巨噬细胞损伤。然后，检测 ox-LDL 处理的巨噬细胞中的铁死亡相关生物标志物和线粒体形态。随后，构建 THP-1 衍生巨噬细胞的 lnc-MRGPRF-6：1 敲低和过表达，并探讨 lnc-MRGPRF-6：1 在 ox-LDL 诱导的铁死亡中的作用。然后成功分离人单核细胞，并用于探讨 lnc-MRGPRF-6：1 在巨噬细胞铁死亡中的作用。同样，构建 lnc-MRGPRF-6：1 敲低和过表达的人单核细胞衍生巨噬细胞，并检测铁死亡相关生物标志物的表达水平。然后进行转录组测序、文献检索以及定量实时聚合酶链反应和 Western blot 检测，以探讨该过程中的特定信号通路。结果表明，lnc-MRGPRF-6：1 可能通过谷胱甘肽过氧化物酶 4（GPX4）调节 ox-LDL 诱导的巨噬细胞铁死亡。最终，在 CAD 患者和对照组的单核细胞衍生巨噬细胞中测量 lnc-MRGPRF-6：1 与 GPX4 的相关性。

结果：ox-LDL 诱导的巨噬细胞损伤涉及铁死亡。lnc-MRGPRF-6：1 的敲低可减轻 ox-LDL 诱导的巨噬细胞铁死亡。同时，lnc-MRGPRF-6：1 的过表达可加重 ox-LDL 诱导的铁死亡。此外，lnc-MRGPRF-6：1 的敲低可减轻 RAS 选择性致死化合物 3（RSL-3）引起的 GPX4 减少。这表明 lnc-MRGPRF-6：1 可能通过抑制 GPX4 诱导巨噬细胞铁死亡。最终，lnc-MRGPRF-6：1 在 CAD 患者的单核细胞衍生巨噬细胞中高表达，并与 GPX4 的表达呈负相关。

结论：lnc-MRGPRF-6：1 可通过抑制 GPX4 促进 ox-LDL 诱导的巨噬细胞铁死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/f74eed743472/MI2023-5513245.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/5a6bf9ea7a86/MI2023-5513245.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/50a592f7f0c7/MI2023-5513245.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/1a54c9430a4e/MI2023-5513245.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/71644f4eb232/MI2023-5513245.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/f74eed743472/MI2023-5513245.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/5a6bf9ea7a86/MI2023-5513245.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/50a592f7f0c7/MI2023-5513245.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/1a54c9430a4e/MI2023-5513245.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/71644f4eb232/MI2023-5513245.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300e/10447047/f74eed743472/MI2023-5513245.005.jpg

相似文献

[1]
lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4.

Mediators Inflamm. 2023

[2]
lnc-MRGPRF-6:1 Promotes M1 Polarization of Macrophage and Inflammatory Response through the TLR4-MyD88-MAPK Pathway.

Mediators Inflamm. 2022

[3]
FNDC5/PPARa Pathway Alleviates THP-1-derived Macrophage Pyroptosis and Its Mechanism.

Altern Ther Health Med. 2023-4

[4]
Novel function of fluvastatin in attenuating oxidized low-density lipoprotein-induced endothelial cell ferroptosis in a glutathione peroxidase4- and cystine-glutamate antiporter-dependent manner.

Exp Ther Med. 2021-11

[5]
Autophagy inhibition and ferroptosis activation during atherosclerosis: Hypoxia-inducible factor 1α inhibitor PX-478 alleviates atherosclerosis by inducing autophagy and suppressing ferroptosis in macrophages.

Biomed Pharmacother. 2023-5

[6]
IDH1 Promotes Foam Cell Formation by Aggravating Macrophage Ferroptosis.

Biology (Basel). 2022-9-23

[7]
CircTM7SF3 contributes to oxidized low-density lipoprotein-induced apoptosis, inflammation and oxidative stress through targeting miR-206/ASPH axis in atherosclerosis cell model in vitro.

BMC Cardiovasc Disord. 2021-2-2

[8]
Silence of long intergenic noncoding RNA HOTAIR ameliorates oxidative stress and inflammation response in ox-LDL-treated human macrophages by upregulating miR-330-5p.

J Cell Physiol. 2018-9-6

[9]
Blockade of NEAT1 represses inflammation response and lipid uptake via modulating miR-342-3p in human macrophages THP-1 cells.

J Cell Physiol. 2018-9-27

[10]
H19 lncRNA triggers ferroptosis, exacerbating ox-LDL-induced artery endothelial cell damage in vitro.

Clin Hemorheol Microcirc. 2024

引用本文的文献

[1]
Exercise in atherosclerosis: its beneficial effects and underlying mechanism.

Front Cell Dev Biol. 2025-8-11

[2]
Ferroptosis-related LncRNAs in diseases.

BMC Biol. 2025-6-6

[3]
Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).

Int J Mol Med. 2025-8

[4]
Progress in the study of the mechanism of ferroptosis in coronary heart disease and clinical intervention strategies.

Front Cardiovasc Med. 2025-4-16

[5]
miR-214-3p Promotes ox-LDL-Induced Macrophages Ferroptosis and Inflammation via GPX4.

J Inflamm Res. 2025-3-17

[6]
The role of ferroptosis-related non-coding RNA in liver fibrosis.

Front Cell Dev Biol. 2024-12-9

[7]
Interaction between macrophages and ferroptosis: Metabolism, function, and diseases.

Chin Med J (Engl). 2024-9-6

[8]
Decoding LncRNA in COPD: Unveiling Prognostic and Diagnostic Power and Their Driving Role in Lung Cancer Progression.

Int J Mol Sci. 2024-8-19

[9]
Non-coding RNA: A key regulator in the Glutathione-GPX4 pathway of ferroptosis.

Noncoding RNA Res. 2024-5-20

[10]
The dance of macrophage death: the interplay between the inevitable and the microenvironment.

Front Immunol. 2024

本文引用的文献

[1]
GPX4-independent ferroptosis-a new strategy in disease's therapy.

Cell Death Discov. 2022-10-30

[2]
Astaxanthin attenuates ferroptosis via Keap1-Nrf2/HO-1 signaling pathways in LPS-induced acute lung injury.

Life Sci. 2022-12-15

[3]
ACSL3 regulates lipid droplet biogenesis and ferroptosis sensitivity in clear cell renal cell carcinoma.

Cancer Metab. 2022-10-3

[4]
Baicalein ameliorates cerebral ischemia-reperfusion injury by inhibiting ferroptosis via regulating GPX4/ACSL4/ACSL3 axis.

Chem Biol Interact. 2022-10-1

[5]
Novel Diagnostic Biomarkers Related to Oxidative Stress and Macrophage Ferroptosis in Atherosclerosis.

Oxid Med Cell Longev. 2022-8-5

[6]
Puerarin Attenuates Oxidative Stress and Ferroptosis via AMPK/PGC1α/Nrf2 Pathway after Subarachnoid Hemorrhage in Rats.

Antioxidants (Basel). 2022-6-27

[7]
Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications.

Cell. 2022-7-7

[8]
The molecular and metabolic landscape of iron and ferroptosis in cardiovascular disease.

Nat Rev Cardiol. 2023-1

[9]
High Level of Uric Acid Promotes Atherosclerosis by Targeting NRF2-Mediated Autophagy Dysfunction and Ferroptosis.

Oxid Med Cell Longev. 2022-4-18

[10]
Disruption of USP9X in macrophages promotes foam cell formation and atherosclerosis.

J Clin Invest. 2022-5-16

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索