• 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

心肌梗死后组织特异性代谢串扰的综合转录组学分析。

Integrative transcriptomic analysis of tissue-specific metabolic crosstalk after myocardial infarction.

机构信息

Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.

Department of Molecular and Clinical Medicine, University of Gothenburg, The Wallenberg Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden.

出版信息

Elife. 2021 May 11;10:e66921. doi: 10.7554/eLife.66921.

DOI:10.7554/eLife.66921
PMID:33972017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8186902/
Abstract

Myocardial infarction (MI) promotes a range of systemic effects, many of which are unknown. Here, we investigated the alterations associated with MI progression in heart and other metabolically active tissues (liver, skeletal muscle, and adipose) in a mouse model of MI (induced by ligating the left ascending coronary artery) and sham-operated mice. We performed a genome-wide transcriptomic analysis on tissue samples obtained 6- and 24 hr post MI or sham operation. By generating tissue-specific biological networks, we observed: (1) dysregulation in multiple biological processes (including immune system, mitochondrial dysfunction, fatty-acid beta-oxidation, and RNA and protein processing) across multiple tissues post MI and (2) tissue-specific dysregulation in biological processes in liver and heart post MI. Finally, we validated our findings in two independent MI cohorts. Overall, our integrative analysis highlighted both common and specific biological responses to MI across a range of metabolically active tissues.

摘要

心肌梗死(MI)会引发一系列全身效应,其中许多效应尚不清楚。在这里,我们研究了 MI 进展相关的改变,该模型是通过结扎左冠状动脉升支构建的,研究对象包括心肌、其他代谢活跃组织(肝脏、骨骼肌和脂肪组织)以及假手术组小鼠。我们对 MI 后 6 小时和 24 小时以及假手术组获得的组织样本进行了全基因组转录组分析。通过构建组织特异性生物网络,我们观察到:(1)MI 后多个组织中多种生物学过程(包括免疫系统、线粒体功能障碍、脂肪酸β氧化以及 RNA 和蛋白质加工)的失调;(2)MI 后肝脏和心脏中生物学过程的组织特异性失调。最后,我们在两个独立的 MI 队列中验证了我们的发现。总的来说,我们的综合分析突出了 MI 在多种代谢活跃组织中的共同和特异性生物学反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/257dd0665d32/elife-66921-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/890c10cc7539/elife-66921-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/0a54155ef935/elife-66921-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/4c2faa7f15b1/elife-66921-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/c6ce70499527/elife-66921-fig1-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/448db6c3f59a/elife-66921-fig1-figsupp4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/54829978ffe1/elife-66921-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/979922e82e64/elife-66921-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/c75d62b5521c/elife-66921-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/eec789f65e45/elife-66921-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/64c554d2ed6e/elife-66921-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/b2070568b587/elife-66921-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/257dd0665d32/elife-66921-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/890c10cc7539/elife-66921-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/0a54155ef935/elife-66921-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/4c2faa7f15b1/elife-66921-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/c6ce70499527/elife-66921-fig1-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/448db6c3f59a/elife-66921-fig1-figsupp4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/54829978ffe1/elife-66921-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/979922e82e64/elife-66921-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/c75d62b5521c/elife-66921-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/eec789f65e45/elife-66921-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/64c554d2ed6e/elife-66921-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/b2070568b587/elife-66921-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7598/8186902/257dd0665d32/elife-66921-fig6.jpg

相似文献

1
Integrative transcriptomic analysis of tissue-specific metabolic crosstalk after myocardial infarction.心肌梗死后组织特异性代谢串扰的综合转录组学分析。
Elife. 2021 May 11;10:e66921. doi: 10.7554/eLife.66921.
2
[A transcriptomic analysis of correlation between mitochondrial function and energy metabolism remodeling in mice with myocardial fibrosis following myocardial infarction].[心肌梗死后心肌纤维化小鼠线粒体功能与能量代谢重塑相关性的转录组学分析]
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Apr 20;44(4):666-674. doi: 10.12122/j.issn.1673-4254.2024.04.07.
3
Dipeptidyl peptidase-4 inhibitor improved exercise capacity and mitochondrial biogenesis in mice with heart failure via activation of glucagon-like peptide-1 receptor signalling.二肽基肽酶-4 抑制剂通过激活胰高血糖素样肽-1 受体信号改善心力衰竭小鼠的运动能力和线粒体生物发生。
Cardiovasc Res. 2016 Sep;111(4):338-47. doi: 10.1093/cvr/cvw182. Epub 2016 Jul 21.
4
Activation of PPARδ signaling improves skeletal muscle oxidative metabolism and endurance function in an animal model of ischemic left ventricular dysfunction.在缺血性左心室功能障碍动物模型中,PPARδ信号通路的激活可改善骨骼肌氧化代谢和耐力功能。
Am J Physiol Heart Circ Physiol. 2015 May 1;308(9):H1078-85. doi: 10.1152/ajpheart.00679.2014. Epub 2015 Feb 20.
5
Effects of exercise training on brain-derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction.运动训练对心肌梗死后大鼠骨骼肌和心脏中脑源性神经营养因子的影响。
Exp Physiol. 2017 Mar 1;102(3):314-328. doi: 10.1113/EP086049.
6
Mapping macrophage polarization over the myocardial infarction time continuum.描绘心肌梗死时间连续体上的巨噬细胞极化。
Basic Res Cardiol. 2018 Jun 4;113(4):26. doi: 10.1007/s00395-018-0686-x.
7
Effects of levosimendan on cardiac gene expression profile and post-infarct cardiac remodelling in diabetic Goto-Kakizaki rats.左西孟旦对糖尿病 Goto-Kakizaki 大鼠心脏基因表达谱及心肌梗死后心脏重构的影响。
Basic Clin Pharmacol Toxicol. 2011 Nov;109(5):387-97. doi: 10.1111/j.1742-7843.2011.00743.x. Epub 2011 Aug 17.
8
Protein acetylation in skeletal muscle mitochondria is involved in impaired fatty acid oxidation and exercise intolerance in heart failure.骨骼肌线粒体中的蛋白质乙酰化与心力衰竭中脂肪酸氧化受损和运动不耐受有关。
J Cachexia Sarcopenia Muscle. 2018 Oct;9(5):844-859. doi: 10.1002/jcsm.12322. Epub 2018 Aug 30.
9
Direct renin inhibitor ameliorates insulin resistance by improving insulin signaling and oxidative stress in the skeletal muscle from post-infarct heart failure in mice.直接肾素抑制剂通过改善胰岛素信号和氧化应激改善心肌梗死后心力衰竭小鼠骨骼肌的胰岛素抵抗。
Eur J Pharmacol. 2016 May 15;779:147-56. doi: 10.1016/j.ejphar.2016.03.022. Epub 2016 Mar 14.
10
Galectin-3 is expressed in the myocardium very early post-myocardial infarction.半乳糖凝集素-3在心肌梗死后极早期就在心肌中表达。
Cardiovasc Pathol. 2015 Jul-Aug;24(4):213-23. doi: 10.1016/j.carpath.2014.12.001. Epub 2014 Dec 9.

引用本文的文献

1
Decoding the Liver-Heart Axis in Cardiometabolic Diseases.解读心脏代谢疾病中的肝心轴
Circ Res. 2025 May 23;136(11):1335-1362. doi: 10.1161/CIRCRESAHA.125.325492. Epub 2025 May 22.
2
Multi-tissue network analysis reveals the effect of JNK inhibition on dietary sucrose-induced metabolic dysfunction in rats.多组织网络分析揭示了JNK抑制对大鼠饮食蔗糖诱导的代谢功能障碍的影响。
Elife. 2025 Feb 11;13:RP98427. doi: 10.7554/eLife.98427.
3
Gene Expression Signatures of Smoking and Acute Myocardial Infarction: A Blood Transcriptome Analysis.

本文引用的文献

1
Inter-organ cross-talk in metabolic syndrome.代谢综合征中的器官间串扰。
Nat Metab. 2019 Dec;1(12):1177-1188. doi: 10.1038/s42255-019-0145-5. Epub 2019 Dec 9.
2
Loss of Filamin C Is Catastrophic for Heart Function.细丝蛋白C的缺失对心脏功能来说是灾难性的。
Circulation. 2020 Mar 10;141(10):869-871. doi: 10.1161/CIRCULATIONAHA.119.044061. Epub 2020 Mar 9.
3
RNA sequencing-based transcriptome profiling of cardiac tissue implicates novel putative disease mechanisms in FLNC-associated arrhythmogenic cardiomyopathy.
吸烟与急性心肌梗死的基因表达特征:一项血液转录组分析
Mediators Inflamm. 2025 Jan 15;2025:2431090. doi: 10.1155/mi/2431090. eCollection 2025.
4
Vitamin A deficiency and male-specific effects on heart function in mice.维生素A缺乏与对小鼠心脏功能的雄性特异性影响
Biochem Biophys Res Commun. 2025 Feb 8;748:151300. doi: 10.1016/j.bbrc.2025.151300. Epub 2025 Jan 9.
5
A combined analysis of bulk RNA-seq and scRNA-seq was performed to investigate the molecular mechanisms associated with the occurrence of myocardial infarction.对 bulk RNA-seq 和 scRNA-seq 进行联合分析,以研究与心肌梗死发生相关的分子机制。
BMC Genomics. 2024 Oct 3;25(1):921. doi: 10.1186/s12864-024-10813-1.
6
Reward system activation improves recovery from acute myocardial infarction.奖励系统的激活可促进急性心肌梗死的恢复。
Nat Cardiovasc Res. 2024 Jul;3(7):841-856. doi: 10.1038/s44161-024-00491-3. Epub 2024 Jul 12.
7
ELF5-Regulated lncRNA-TTN-AS1 Alleviates Myocardial Cell Injury via Recruiting PCBP2 to Increase CDK6 Stability in Myocardial Infarction.ELF5 调控的长链非编码 RNA-TTN-AS1 通过募集 PCBP2 增加 CDK6 稳定性来减轻心肌细胞损伤在心肌梗死中。
Mol Cell Biol. 2024;44(8):303-315. doi: 10.1080/10985549.2024.2374083. Epub 2024 Jul 21.
8
Novel Fibrillar and Non-Fibrillar Collagens Involved in Fibrotic Scar Formation after Myocardial Infarction.新型纤维状和非纤维状胶原蛋白在心肌梗死后纤维化瘢痕形成中的作用。
Int J Mol Sci. 2024 Jun 16;25(12):6625. doi: 10.3390/ijms25126625.
9
KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy.KDM8通过表观遗传方式调控心脏代谢,以防止扩张型心肌病的发生。
Nat Cardiovasc Res. 2023;2(2):174-191. doi: 10.1038/s44161-023-00214-0. Epub 2023 Feb 13.
10
Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis.新型靶点调节梗死后内皮细胞和血管生成的作用:RNA 测序分析。
Int J Mol Sci. 2023 Oct 28;24(21):15698. doi: 10.3390/ijms242115698.
基于 RNA 测序的心脏组织转录组谱分析提示 FLNC 相关心律失常性心肌病的新潜在疾病机制。
Int J Cardiol. 2020 Mar 1;302:124-130. doi: 10.1016/j.ijcard.2019.12.002. Epub 2019 Dec 6.
4
The human secretome.人类分泌组。
Sci Signal. 2019 Nov 26;12(609):eaaz0274. doi: 10.1126/scisignal.aaz0274.
5
Non-alcoholic fatty liver disease and risk of incident acute myocardial infarction and stroke: findings from matched cohort study of 18 million European adults.非酒精性脂肪性肝病与急性心肌梗死和卒中发病风险的关系:来自 1800 万欧洲成年人匹配队列研究的结果。
BMJ. 2019 Oct 8;367:l5367. doi: 10.1136/bmj.l5367.
6
Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.心脏肥大与心力衰竭中的葡萄糖代谢
J Am Heart Assoc. 2019 Jun 18;8(12):e012673. doi: 10.1161/JAHA.119.012673. Epub 2019 Jun 12.
7
From Louvain to Leiden: guaranteeing well-connected communities.从鲁汶到莱顿:保障互联互通的社区。
Sci Rep. 2019 Mar 26;9(1):5233. doi: 10.1038/s41598-019-41695-z.
8
Discovery of therapeutic agents for prostate cancer using genome-scale metabolic modeling and drug repositioning.利用基因组规模代谢建模和药物重定位发现治疗前列腺癌的药物。
EBioMedicine. 2019 Apr;42:386-396. doi: 10.1016/j.ebiom.2019.03.009. Epub 2019 Mar 21.
9
Transcriptomics of cardiac biopsies reveals differences in patients with or without diagnostic parameters for heart failure with preserved ejection fraction.心脏活检转录组学揭示了射血分数保留的心力衰竭患者是否具有诊断参数的差异。
Sci Rep. 2019 Feb 28;9(1):3179. doi: 10.1038/s41598-019-39445-2.
10
Characterization of heterogeneous redox responses in hepatocellular carcinoma patients using network analysis.利用网络分析对肝癌患者的异质氧化还原反应进行特征描述。
EBioMedicine. 2019 Feb;40:471-487. doi: 10.1016/j.ebiom.2018.12.057. Epub 2018 Dec 31.