• 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

心肌肥大受到miR-541的负调控。

Cardiac hypertrophy is negatively regulated by miR-541.

作者信息

Liu F, Li N, Long B, Fan Y-Y, Liu C-Y, Zhou Q-Y, Murtaza I, Wang K, Li P-F

机构信息

Division of Cardiovascular Research, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.

Department of Pharmacology, University of California, Irvine, CA 92697, USA.

出版信息

Cell Death Dis. 2014 Apr 10;5(4):e1171. doi: 10.1038/cddis.2014.141.

DOI:10.1038/cddis.2014.141
PMID:24722296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5424117/
Abstract

Heart failure is a leading cause of death in aging population. Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading, but continuous cardiac hypertrophy is able to induce heart failure. We found that the level of miR-541 was decreased in angiotensin II (Ang-II) treated cardiomyocytes. Enforced expression of miR-541 resulted in a reduced hypertrophic phenotype upon Ang-II treatment in cellular models. In addition, we generated miR-541 transgenic mice that exhibited a reduced hypertrophic response upon Ang-II treatment. Furthermore, we found miR-541 is the target of microphthalmia-associated transcription factor (MITF) in the hypertrophic pathway and MITF can negatively regulate the expression of miR-541 at the transcriptional levels. MITF(ce/ce) mice exhibited a reduced hypertrophic phenotype upon Ang-II treatment. Knockdown of MITF also results in a reduction of hypertrophic responses after Ang-II treatment. Knockdown of miR-541 can block the antihypertrophic effect of MITF knockdown in cardiomyocytes upon Ang-II treatment. This indicates that the effect of MITF on cardiac hypertrophy relies on the regulation of miR-541. Our present study reveals a novel cardiac hypertrophy regulating pathway that was composed of miR-541 and MITF. Modulation of their levels may provide a new approach for tackling cardiac hypertrophy.

摘要

心力衰竭是老年人群死亡的主要原因。心脏肥大是心脏对心脏负荷过重的一种适应性反应，但持续的心脏肥大能够诱发心力衰竭。我们发现，在血管紧张素II（Ang-II）处理的心肌细胞中，miR-541的水平降低。在细胞模型中，过表达miR-541会导致Ang-II处理后肥大表型减弱。此外，我们构建了miR-541转基因小鼠，其在Ang-II处理后表现出减弱的肥大反应。此外，我们发现miR-541是肥大通路中小眼相关转录因子（MITF）的靶标，并且MITF可以在转录水平上负向调节miR-541的表达。MITF(ce/ce)小鼠在Ang-II处理后表现出减弱的肥大表型。敲低MITF也会导致Ang-II处理后肥大反应减弱。敲低miR-541可以阻断MITF敲低对Ang-II处理的心肌细胞的抗肥大作用。这表明MITF对心脏肥大的作用依赖于对miR-541的调节。我们目前的研究揭示了一条由miR-541和MITF组成的新型心脏肥大调节通路。调节它们的水平可能为解决心脏肥大提供一种新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/1eb20cd451d5/cddis2014141f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/84a6b58270ec/cddis2014141f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/9063f3ce6f35/cddis2014141f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/db5ee5954429/cddis2014141f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/d117b4ed7b45/cddis2014141f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/20044907f0d0/cddis2014141f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/1eb20cd451d5/cddis2014141f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/84a6b58270ec/cddis2014141f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/9063f3ce6f35/cddis2014141f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/db5ee5954429/cddis2014141f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/d117b4ed7b45/cddis2014141f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/20044907f0d0/cddis2014141f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c312/5424117/1eb20cd451d5/cddis2014141f6.jpg

相似文献

1
Cardiac hypertrophy is negatively regulated by miR-541.心肌肥大受到miR-541的负调控。
Cell Death Dis. 2014 Apr 10;5(4):e1171. doi: 10.1038/cddis.2014.141.
2
The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489.长链非编码 RNA CHRF 通过靶向 miR-489 调节心肌肥厚。
Circ Res. 2014 Apr 25;114(9):1377-88. doi: 10.1161/CIRCRESAHA.114.302476. Epub 2014 Feb 20.
3
MITF interacts with the SWI/SNF subunit, BRG1, to promote GATA4 expression in cardiac hypertrophy.小眼畸形相关转录因子（MITF）与SWI/SNF亚基BRG1相互作用，以促进心肌肥厚中GATA4的表达。
J Mol Cell Cardiol. 2015 Nov;88:101-10. doi: 10.1016/j.yjmcc.2015.09.010. Epub 2015 Sep 24.
4
Myocyte-specific enhancer factor 2C: a novel target gene of miR-214-3p in suppressing angiotensin II-induced cardiomyocyte hypertrophy.肌细胞特异性增强因子 2C：miR-214-3p 抑制血管紧张素 II 诱导的心肌细胞肥大的新靶基因。
Sci Rep. 2016 Oct 31;6:36146. doi: 10.1038/srep36146.
5
MicroRNA-214 contributes to Ang II-induced cardiac hypertrophy by targeting SIRT3 to provoke mitochondrial malfunction.MicroRNA-214 通过靶向 SIRT3 引发线粒体功能障碍促进 Ang II 诱导的心肌肥厚。
Acta Pharmacol Sin. 2021 Sep;42(9):1422-1436. doi: 10.1038/s41401-020-00563-7. Epub 2020 Nov 27.
6
MiR-30e-5p is sponged by Kcnq1ot1 and represses Angiotensin II-induced hypertrophic phenotypes in cardiomyocytes by targeting ADAM9.miR-30e-5p 通过海绵吸附 Kcnq1ot1，通过靶向 ADAM9 抑制心肌细胞中血管紧张素 II 诱导的肥大表型。
Exp Cell Res. 2020 Sep 15;394(2):112140. doi: 10.1016/j.yexcr.2020.112140. Epub 2020 Jun 12.
7
Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7.硫氧还蛋白 1 通过上调 miR-98/let-7 负调控血管紧张素Ⅱ诱导的心肌肥厚。
Circ Res. 2011 Feb 4;108(3):305-13. doi: 10.1161/CIRCRESAHA.110.228437. Epub 2010 Dec 23.
8
MicroRNA-92b-3p suppresses angiotensin II-induced cardiomyocyte hypertrophy via targeting HAND2.miR-92b-3p 通过靶向 HAND2 抑制血管紧张素 II 诱导的心肌细胞肥大。
Life Sci. 2019 Sep 1;232:116635. doi: 10.1016/j.lfs.2019.116635. Epub 2019 Jul 5.
9
miR-34a modulates angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity.微小RNA-34a通过直接抑制自噬相关蛋白9A（ATG9A）的表达和自噬活性来调节血管紧张素II诱导的心肌肥大。
PLoS One. 2014 Apr 11;9(4):e94382. doi: 10.1371/journal.pone.0094382. eCollection 2014.
10
MiR-181a mediates Ang II-induced myocardial hypertrophy by mediating autophagy.miR-181a 通过介导自噬来介导 Ang II 诱导的心肌肥大。
Eur Rev Med Pharmacol Sci. 2017 Dec;21(23):5462-5470. doi: 10.26355/eurrev_201712_13936.

引用本文的文献

1
Epigenetic Mechanisms in Heart Diseases.心脏病中的表观遗传机制
Rev Cardiovasc Med. 2025 Jul 30;26(7):38696. doi: 10.31083/RCM38696. eCollection 2025 Jul.
2
Obesity and Heart Failure: Mechanistic Insights and the Regulatory Role of MicroRNAs.肥胖与心力衰竭：机制洞察及微小RNA的调节作用
Genes (Basel). 2025 May 28;16(6):647. doi: 10.3390/genes16060647.
3
Altered expression of miR-375 and miR-541 in type 2 diabetes patients with and without coronary artery disease (CAD): the potential of miR-375 as a CAD biomarker.

本文引用的文献

1
Angiotensin II-derived reactive oxygen species promote angiogenesis in human late endothelial progenitor cells through heme oxygenase-1 via ERK1/2 and AKT/PI3K pathways.血管紧张素II衍生的活性氧通过血红素加氧酶-1经ERK1/2和AKT/PI3K途径促进人晚期内皮祖细胞的血管生成。
Inflammation. 2014 Jun;37(3):858-70. doi: 10.1007/s10753-013-9806-9.
2
High-throughput screens identify microRNAs essential for HER2 positive breast cancer cell growth.高通量筛选鉴定出对HER2阳性乳腺癌细胞生长至关重要的微小RNA。
Mol Oncol. 2014 Feb;8(1):93-104. doi: 10.1016/j.molonc.2013.10.001. Epub 2013 Oct 11.
3
miR-874 regulates myocardial necrosis by targeting caspase-8.
伴有和不伴有冠状动脉疾病（CAD）的2型糖尿病患者中miR-375和miR-541的表达改变：miR-375作为CAD生物标志物的潜力
J Diabetes Metab Disord. 2024 Mar 7;23(1):1101-1106. doi: 10.1007/s40200-024-01391-w. eCollection 2024 Jun.
4
Genetic architecture of heart failure with preserved versus reduced ejection fraction.保留射血分数与降低射血分数心力衰竭的遗传结构。
Nat Commun. 2022 Dec 14;13(1):7753. doi: 10.1038/s41467-022-35323-0.
5
Platelet membrane-camouflaged nanoparticles carry microRNA inhibitor against myocardial ischaemia‒reperfusion injury.血小板膜伪装纳米颗粒携带 microRNA 抑制剂对抗心肌缺血再灌注损伤。
J Nanobiotechnology. 2022 Oct 4;20(1):434. doi: 10.1186/s12951-022-01639-8.
6
Sinomenine ameliorates cardiac hypertrophy by activating Nrf2/ARE signaling pathway.青藤碱通过激活 Nrf2/ARE 信号通路改善心肌肥厚。
Bioengineered. 2021 Dec;12(2):12778-12788. doi: 10.1080/21655979.2021.2000195.
7
Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology.心肌梗死：微小RNA在心肌病理中的保护作用
Front Cardiovasc Med. 2021 Mar 5;8:631817. doi: 10.3389/fcvm.2021.631817. eCollection 2021.
8
The Role of Oxidative Stress in Cardiovascular Aging and Cardiovascular Diseases.氧化应激在心血管衰老和心血管疾病中的作用
Life (Basel). 2021 Jan 15;11(1):60. doi: 10.3390/life11010060.
9
Regulation of Long Non-coding RNAs and MicroRNAs in Heart Disease: Insight Into Mechanisms and Therapeutic Approaches.长链非编码RNA和微小RNA在心脏病中的调控：对机制和治疗方法的洞察
Front Physiol. 2020 Jul 10;11:798. doi: 10.3389/fphys.2020.00798. eCollection 2020.
10
Substance P Administered after Myocardial Infarction Upregulates Microphthalmia-Associated Transcription Factor, GATA4, and the Expansion of c-Kit Cells.心肌梗死后给予P物质可上调小眼相关转录因子、GATA4以及c-Kit细胞的扩增。
Stem Cells Int. 2020 Feb 10;2020:1835950. doi: 10.1155/2020/1835950. eCollection 2020.
miR-874 通过靶向半胱天冬酶-8 调节心肌坏死。
Cell Death Dis. 2013 Jul 4;4(7):e709. doi: 10.1038/cddis.2013.233.
4
Angiotensin II upregulates K(Ca)3.1 channels and stimulates cell proliferation in rat cardiac fibroblasts.血管紧张素 II 上调 K(Ca)3.1 通道并刺激大鼠心肌成纤维细胞增殖。
Biochem Pharmacol. 2013 May 15;85(10):1486-94. doi: 10.1016/j.bcp.2013.02.032. Epub 2013 Mar 7.
5
Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice.心肌细胞中 miR-27b 的过表达可诱导小鼠心脏肥大和功能障碍。
Cell Res. 2012 Mar;22(3):516-27. doi: 10.1038/cr.2011.132. Epub 2011 Aug 16.
6
miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes.miR-24 抑制凋亡并抑制小鼠心肌细胞中的 Bim。
J Exp Med. 2011 Mar 14;208(3):549-60. doi: 10.1084/jem.20101547. Epub 2011 Mar 7.
7
miR-499 regulates mitochondrial dynamics by targeting calcineurin and dynamin-related protein-1.miR-499 通过靶向钙调神经磷酸酶和动力相关蛋白 1 调节线粒体动力学。
Nat Med. 2011 Jan;17(1):71-8. doi: 10.1038/nm.2282. Epub 2010 Dec 26.
8
Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7.硫氧还蛋白 1 通过上调 miR-98/let-7 负调控血管紧张素Ⅱ诱导的心肌肥厚。
Circ Res. 2011 Feb 4;108(3):305-13. doi: 10.1161/CIRCRESAHA.110.228437. Epub 2010 Dec 23.
9
MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling.MicroRNA-199b 通过自动扩增环靶向核激酶 Dyrk1a，促进钙调磷酸酶/NFAT 信号传导。
Nat Cell Biol. 2010 Dec;12(12):1220-7. doi: 10.1038/ncb2126. Epub 2010 Nov 21.
10
MicroRNA-494 targeting both proapoptotic and antiapoptotic proteins protects against ischemia/reperfusion-induced cardiac injury.microRNA-494 通过靶向促凋亡和抗凋亡蛋白来保护心脏免受缺血/再灌注损伤。
Circulation. 2010 Sep 28;122(13):1308-18. doi: 10.1161/CIRCULATIONAHA.110.964684. Epub 2010 Sep 13.