• 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

人类主动脉瓣狭窄的代谢组学特征

Metabolomic Signature of Human Aortic Valve Stenosis.

作者信息

Surendran Arun, Edel Andrea, Chandran Mahesh, Bogaert Pascal, Hassan-Tash Pedram, Kumar Asokan Aneesh, Hiebert Brett, Solati Zahra, Sandhawalia Shubhkarman, Raabe Michael, Kass Malek, Shah Ashish, Jassal Davinder S, Jaleel Abdul, Ravandi Amir

机构信息

Cardiovascular Lipidomics Laboratory, St. Boniface Hospital, Albrechtsen Research Centre, Winnipeg, Manitoba, Canada.

Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.

出版信息

JACC Basic Transl Sci. 2020 Dec 16;5(12):1163-1177. doi: 10.1016/j.jacbts.2020.10.001. eCollection 2020 Dec.

DOI:10.1016/j.jacbts.2020.10.001
PMID:33426374
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7775961/
Abstract

This study outlines the first step toward creating the metabolite atlas of human calcified aortic valves by identifying the expression of metabolites and metabolic pathways involved at various stages of calcific aortic valve stenosis progression. Untargeted analysis identified 72 metabolites and lipids that were significantly altered (p < 0.01) across different stages of disease progression. Of these metabolites and lipids, the levels of lysophosphatidic acid were shown to correlate with faster hemodynamic progression and could select patients at risk for faster progression rate.

摘要

本研究通过鉴定钙化性主动脉瓣狭窄进展各阶段所涉及的代谢物表达和代谢途径,概述了创建人类钙化主动脉瓣代谢物图谱的第一步。非靶向分析鉴定出72种在疾病进展不同阶段有显著变化(p < 0.01)的代谢物和脂质。在这些代谢物和脂质中,溶血磷脂酸水平与更快的血流动力学进展相关,并且可以筛选出进展速度较快的高危患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/d2712c183123/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/b93b432b980c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/5aa8606ed3d4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/5bb14e790c22/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/e90092919eb1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/dc6d1897c0fb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/c403983fccfa/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/20a11e623a35/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/856d6b00da1b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/d2712c183123/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/b93b432b980c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/5aa8606ed3d4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/5bb14e790c22/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/e90092919eb1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/dc6d1897c0fb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/c403983fccfa/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/20a11e623a35/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/856d6b00da1b/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ded5/7775961/d2712c183123/gr8.jpg

相似文献

1
Metabolomic Signature of Human Aortic Valve Stenosis.人类主动脉瓣狭窄的代谢组学特征
JACC Basic Transl Sci. 2020 Dec 16;5(12):1163-1177. doi: 10.1016/j.jacbts.2020.10.001. eCollection 2020 Dec.
2
Interaction of Autotaxin With Lipoprotein(a) in Patients With Calcific Aortic Valve Stenosis.钙化性主动脉瓣狭窄患者中自分泌运动因子与脂蛋白(a)的相互作用。
JACC Basic Transl Sci. 2020 Aug 26;5(9):888-897. doi: 10.1016/j.jacbts.2020.06.012. eCollection 2020 Sep.
3
Steady flow hemodynamic and energy loss measurements in normal and simulated calcified tricuspid and bicuspid aortic valves.正常及模拟钙化三尖瓣和二尖瓣主动脉瓣的稳流血液动力学及能量损失测量
J Biomech Eng. 2014 Apr;136(4). doi: 10.1115/1.4026575.
4
Autotaxin inhibition attenuates the aortic valve calcification by suppressing inflammation-driven fibro-calcific remodeling of valvular interstitial cells.自分泌酶抑制通过抑制炎症驱动的瓣膜间质细胞纤维钙化重塑来减轻主动脉瓣钙化。
BMC Med. 2024 Mar 14;22(1):122. doi: 10.1186/s12916-024-03342-x.
5
Autotaxin Derived From Lipoprotein(a) and Valve Interstitial Cells Promotes Inflammation and Mineralization of the Aortic Valve.脂蛋白(a)衍生的自分泌酶和瓣间充质细胞促进主动脉瓣炎症和钙化。
Circulation. 2015 Aug 25;132(8):677-90. doi: 10.1161/CIRCULATIONAHA.115.016757. Epub 2015 Jul 29.
6
Ex vivo assessment of valve thickness/calcification of patients with calcific aortic stenosis in relation to in vivo clinical outcomes.钙化性主动脉瓣狭窄患者瓣膜厚度/钙化的体外评估与体内临床结局的关系。
J Mech Behav Biomed Mater. 2017 Oct;74:324-332. doi: 10.1016/j.jmbbm.2017.06.020. Epub 2017 Jun 22.
7
Activated platelets promote an osteogenic programme and the progression of calcific aortic valve stenosis.活化的血小板促进成骨程序和钙化性主动脉瓣狭窄的进展。
Eur Heart J. 2019 May 1;40(17):1362-1373. doi: 10.1093/eurheartj/ehy696.
8
Prediction of Aortic Stenosis Progression by F-FDG and F-NaF PET/CT in Different Aortic Valve Phenotypes.F-FDG和F-NaF PET/CT对不同主动脉瓣表型的主动脉瓣狭窄进展的预测
Front Pharmacol. 2022 May 24;13:909975. doi: 10.3389/fphar.2022.909975. eCollection 2022.
9
Lipoprotein(a) Associated Molecules are Prominent Components in Plasma and Valve Leaflets in Calcific Aortic Valve Stenosis.脂蛋白(a)相关分子是钙化性主动脉瓣狭窄患者血浆和瓣膜小叶中的主要成分。
JACC Basic Transl Sci. 2017 Jun;2(3):229-240. doi: 10.1016/j.jacbts.2017.02.004. Epub 2017 Jun 26.
10
Autotaxin interacts with lipoprotein(a) and oxidized phospholipids in predicting the risk of calcific aortic valve stenosis in patients with coronary artery disease.自分泌酶与脂蛋白 (a) 和氧化型磷脂在预测冠心病患者钙化性主动脉瓣狭窄风险中的相互作用。
J Intern Med. 2016 Nov;280(5):509-517. doi: 10.1111/joim.12519. Epub 2016 May 30.

引用本文的文献

1
Sex-specific lipidomic signatures in aortic valve disease reflect differential fibro-calcific progression.主动脉瓣疾病中的性别特异性脂质组学特征反映了不同的纤维钙化进展。
Nat Commun. 2025 Jun 3;16(1):5163. doi: 10.1038/s41467-025-60411-2.
2
Conjugated bile acids are elevated in severe calcific aortic valve stenosis.在严重钙化性主动脉瓣狭窄中,结合胆汁酸水平升高。
J Lipid Res. 2025 Jun;66(6):100830. doi: 10.1016/j.jlr.2025.100830. Epub 2025 May 22.
3
Circulating Plasma Proteins in Aortic Stenosis: Associations With Severity, Myocardial Response, and Clinical Outcomes.

本文引用的文献

1
Lipoprotein(a) and Oxidized Phospholipids Promote Valve Calcification in Patients With Aortic Stenosis.脂蛋白(a)和氧化磷脂促进主动脉瓣狭窄患者的瓣膜钙化。
J Am Coll Cardiol. 2019 May 7;73(17):2150-2162. doi: 10.1016/j.jacc.2019.01.070.
2
Autotaxin and Lipoprotein Metabolism in Calcific Aortic Valve Disease.自分泌运动因子与钙化性主动脉瓣疾病中的脂蛋白代谢
Front Cardiovasc Med. 2019 Mar 1;6:18. doi: 10.3389/fcvm.2019.00018. eCollection 2019.
3
Autotaxin, bile acid profile and effect of ileal bile acid transporter inhibition in primary biliary cholangitis patients with pruritus.
循环血浆蛋白在主动脉瓣狭窄中的作用:与严重程度、心肌反应和临床结局的关系。
J Am Heart Assoc. 2024 Oct;13(19):e035486. doi: 10.1161/JAHA.124.035486. Epub 2024 Sep 30.
4
High-Throughput Metabolomics Applications in Pathogenesis and Diagnosis of Valvular Heart Disease.高通量代谢组学在心脏瓣膜病发病机制和诊断中的应用
Rev Cardiovasc Med. 2023 Jun 8;24(6):169. doi: 10.31083/j.rcm2406169. eCollection 2023 Jun.
5
Type 2 Diabetes, Circulating Metabolites, and Calcific Aortic Valve Stenosis: A Mendelian Randomization Study.2型糖尿病、循环代谢物与钙化性主动脉瓣狭窄:一项孟德尔随机化研究
Metabolites. 2024 Jul 13;14(7):385. doi: 10.3390/metabo14070385.
6
Insights into the Inherited Basis of Valvular Heart Disease.瓣膜性心脏病遗传基础的研究进展。
Curr Cardiol Rep. 2024 May;26(5):381-392. doi: 10.1007/s11886-024-02041-6. Epub 2024 Apr 6.
7
Comprehensive Metabolomic Analysis of Human Heart Tissue Enabled by Parallel Metabolite Extraction and High-Resolution Mass Spectrometry.基于平行代谢物提取和高分辨率质谱的人心肌组织综合代谢组学分析。
Anal Chem. 2024 Apr 16;96(15):5781-5789. doi: 10.1021/acs.analchem.3c04353. Epub 2024 Apr 3.
8
Challenges and Opportunities in Valvular Heart Disease: From Molecular Mechanisms to the Community.心脏瓣膜病的挑战与机遇:从分子机制到社区
Arterioscler Thromb Vasc Biol. 2024 Apr;44(4):763-767. doi: 10.1161/ATVBAHA.123.319563. Epub 2024 Mar 27.
9
Specific Multiomic Profiling in Aortic Stenosis in Bicuspid Aortic Valve Disease.二叶式主动脉瓣疾病中主动脉瓣狭窄的特异性多组学分析
Biomedicines. 2024 Feb 6;12(2):380. doi: 10.3390/biomedicines12020380.
10
Metabolic systems approaches update molecular insights of clinical phenotypes and cardiovascular risk in patients with homozygous familial hypercholesterolemia.代谢系统方法更新了对纯合家族性高胆固醇血症患者临床表型和心血管风险的分子认识。
BMC Med. 2023 Jul 27;21(1):275. doi: 10.1186/s12916-023-02967-8.
原发性胆汁性胆管炎瘙痒患者的自分泌酶、胆汁酸谱和回肠胆汁酸转运体抑制作用。
Liver Int. 2019 May;39(5):967-975. doi: 10.1111/liv.14069. Epub 2019 Feb 25.
4
Activated platelets promote an osteogenic programme and the progression of calcific aortic valve stenosis.活化的血小板促进成骨程序和钙化性主动脉瓣狭窄的进展。
Eur Heart J. 2019 May 1;40(17):1362-1373. doi: 10.1093/eurheartj/ehy696.
5
Cardiovascular Metabolomics.心血管代谢组学。
Circ Res. 2018 Apr 27;122(9):1238-1258. doi: 10.1161/CIRCRESAHA.117.311002.
6
Spatiotemporal Multi-Omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease.时空多组学图谱绘制揭示了主动脉瓣疾病相关的分子图谱和调控网络。
Circulation. 2018 Jul 24;138(4):377-393. doi: 10.1161/CIRCULATIONAHA.117.032291.
7
From correlation to causation: analysis of metabolomics data using systems biology approaches.从相关性到因果关系:运用系统生物学方法分析代谢组学数据
Metabolomics. 2018;14(4):37. doi: 10.1007/s11306-018-1335-y. Epub 2018 Feb 27.
8
Lipoprotein(a) Associated Molecules are Prominent Components in Plasma and Valve Leaflets in Calcific Aortic Valve Stenosis.脂蛋白(a)相关分子是钙化性主动脉瓣狭窄患者血浆和瓣膜小叶中的主要成分。
JACC Basic Transl Sci. 2017 Jun;2(3):229-240. doi: 10.1016/j.jacbts.2017.02.004. Epub 2017 Jun 26.
9
Comparative study of bicuspid vs. tricuspid aortic valve stenosis.二叶式主动脉瓣与三叶式主动脉瓣狭窄的对比研究。
Eur Heart J Cardiovasc Imaging. 2018 Jan 1;19(1):3-8. doi: 10.1093/ehjci/jex211.
10
2017 ESC/EACTS Guidelines for the management of valvular heart disease.2017年欧洲心脏病学会/欧洲心胸外科学会瓣膜性心脏病管理指南。
Eur Heart J. 2017 Sep 21;38(36):2739-2791. doi: 10.1093/eurheartj/ehx391.