Suppr超能文献

动脉粥样硬化中的生物力学因素:机制与临床意义

Biomechanical factors in atherosclerosis: mechanisms and clinical implications.

作者信息

Kwak Brenda R, Bäck Magnus, Bochaton-Piallat Marie-Luce, Caligiuri Giuseppina, Daemen Mat J A P, Davies Peter F, Hoefer Imo E, Holvoet Paul, Jo Hanjoong, Krams Rob, Lehoux Stephanie, Monaco Claudia, Steffens Sabine, Virmani Renu, Weber Christian, Wentzel Jolanda J, Evans Paul C

机构信息

Department of Pathology and Immunology, University of Geneva, CMU, Rue Michel-Servet 1, CH-1211 Geneva, Switzerland

Karolinska Institutet, Stockholm, Sweden.

出版信息

Eur Heart J. 2014 Nov 14;35(43):3013-20, 3020a-3020d. doi: 10.1093/eurheartj/ehu353. Epub 2014 Sep 17.

Abstract

Blood vessels are exposed to multiple mechanical forces that are exerted on the vessel wall (radial, circumferential and longitudinal forces) or on the endothelial surface (shear stress). The stresses and strains experienced by arteries influence the initiation of atherosclerotic lesions, which develop at regions of arteries that are exposed to complex blood flow. In addition, plaque progression and eventually plaque rupture is influenced by a complex interaction between biological and mechanical factors-mechanical forces regulate the cellular and molecular composition of plaques and, conversely, the composition of plaques determines their ability to withstand mechanical load. A deeper understanding of these interactions is essential for designing new therapeutic strategies to prevent lesion development and promote plaque stabilization. Moreover, integrating clinical imaging techniques with finite element modelling techniques allows for detailed examination of local morphological and biomechanical characteristics of atherosclerotic lesions that may be of help in prediction of future events. In this ESC Position Paper on biomechanical factors in atherosclerosis, we summarize the current 'state of the art' on the interface between mechanical forces and atherosclerotic plaque biology and identify potential clinical applications and key questions for future research.

摘要

血管会受到多种施加于血管壁(径向、周向和纵向力)或内皮表面(剪切应力)的机械力作用。动脉所经历的应力和应变会影响动脉粥样硬化病变的起始,这些病变会在暴露于复杂血流的动脉区域发展。此外,斑块进展以及最终的斑块破裂受到生物学和机械因素之间复杂相互作用的影响——机械力调节斑块的细胞和分子组成,反之,斑块的组成决定了它们承受机械负荷的能力。深入理解这些相互作用对于设计预防病变发展和促进斑块稳定的新治疗策略至关重要。此外,将临床成像技术与有限元建模技术相结合,可以详细检查动脉粥样硬化病变的局部形态和生物力学特征,这可能有助于预测未来事件。在这份关于动脉粥样硬化生物力学因素的欧洲心脏病学会立场文件中,我们总结了机械力与动脉粥样硬化斑块生物学之间界面的当前“最新技术水平”,并确定了潜在的临床应用以及未来研究的关键问题。

相似文献

1
Biomechanical factors in atherosclerosis: mechanisms and clinical implications.
Eur Heart J. 2014 Nov 14;35(43):3013-20, 3020a-3020d. doi: 10.1093/eurheartj/ehu353. Epub 2014 Sep 17.
2
Biomechanical stress in coronary atherosclerosis: emerging insights from computational modelling.
Eur Heart J. 2017 Jan 7;38(2):81-92. doi: 10.1093/eurheartj/ehv689.
3
Shear stress in atherosclerotic plaque determination.
DNA Cell Biol. 2014 Dec;33(12):830-8. doi: 10.1089/dna.2014.2480.
4
Compressive mechanical properties of atherosclerotic plaques--indentation test to characterise the local anisotropic behaviour.
J Biomech. 2014 Mar 3;47(4):784-92. doi: 10.1016/j.jbiomech.2014.01.018. Epub 2014 Jan 13.
5
Role of biomechanical forces in the natural history of coronary atherosclerosis.
Nat Rev Cardiol. 2016 Apr;13(4):210-20. doi: 10.1038/nrcardio.2015.203. Epub 2016 Jan 29.
6
Effects of mechanical properties and atherosclerotic artery size on biomechanical plaque disruption - mouse vs. human.
J Biomech. 2014 Mar 3;47(4):765-72. doi: 10.1016/j.jbiomech.2014.01.020. Epub 2014 Jan 13.
7
Thin-cap fibroatheroma rupture is associated with a fine interplay of shear and wall stress.
Arterioscler Thromb Vasc Biol. 2014 Oct;34(10):2224-31. doi: 10.1161/ATVBAHA.114.303426. Epub 2014 Jul 24.
8
Optical measurement of arterial mechanical properties: from atherosclerotic plaque initiation to rupture.
J Biomed Opt. 2013 Dec;18(12):121507. doi: 10.1117/1.JBO.18.12.121507.
9
Endothelial autophagic flux hampers atherosclerotic lesion development.
Autophagy. 2018;14(1):173-175. doi: 10.1080/15548627.2017.1395114. Epub 2018 Jan 29.
10
Thrombosis formation on atherosclerotic lesions and plaque rupture.
J Intern Med. 2014 Dec;276(6):618-32. doi: 10.1111/joim.12296. Epub 2014 Sep 25.

引用本文的文献

1
Current status and challenges of multi-omics research using animal models of atherosclerosis.
J Mol Cell Cardiol Plus. 2025 Jul 10;13:100476. doi: 10.1016/j.jmccpl.2025.100476. eCollection 2025 Sep.
2
12/15-lipoxygenase mediates disturbed flow-induced endothelial dysfunction and atherosclerosis.
Mol Med. 2025 Jul 15;31(1):257. doi: 10.1186/s10020-025-01297-0.
3
Hemodynamic changes and their relationship with white matter hyperintensities in CSVD patients with cognitive impairment: a 4D flow study.
Front Aging Neurosci. 2025 Jun 18;17:1578288. doi: 10.3389/fnagi.2025.1578288. eCollection 2025.
4
Aortic Valve Defect as an Independent Risk Factor for Endothelial Dysfunction.
Cells. 2025 Jun 11;14(12):885. doi: 10.3390/cells14120885.
5
Impact of alcohol consumption on atherosclerosis: a systematic review and meta-analysis.
Front Nutr. 2025 Apr 30;12:1563759. doi: 10.3389/fnut.2025.1563759. eCollection 2025.
7
Anatomical Variations and Morphometry of Carotid Sinus: A Computed Tomography Study.
Tomography. 2025 Apr 7;11(4):45. doi: 10.3390/tomography11040045.
8
The Role of 4D Flow MRI-derived Wall Shear Stress in Aortic Disease: A Comprehensive Review.
Rev Cardiovasc Med. 2025 Mar 5;26(3):26735. doi: 10.31083/RCM26735. eCollection 2025 Mar.
10
Advancements in Coronary Bifurcation Stenting Techniques: Insights From Computational and Bench Testing Studies.
Int J Numer Method Biomed Eng. 2025 Mar;41(3):e70000. doi: 10.1002/cnm.70000.

本文引用的文献

2
Emerging topic: flow-related epigenetic regulation of endothelial phenotype through DNA methylation.
Vascul Pharmacol. 2014 Aug;62(2):88-93. doi: 10.1016/j.vph.2014.05.007. Epub 2014 May 27.
3
Flow-dependent epigenetic DNA methylation regulates endothelial gene expression and atherosclerosis.
J Clin Invest. 2014 Jul;124(7):3187-99. doi: 10.1172/JCI74792. Epub 2014 May 27.
4
Hemodynamic disturbed flow induces differential DNA methylation of endothelial Kruppel-Like Factor 4 promoter in vitro and in vivo.
Circ Res. 2014 Jun 20;115(1):32-43. doi: 10.1161/CIRCRESAHA.115.303883. Epub 2014 Apr 22.
5
Disturbed flow promotes endothelial senescence via a p53-dependent pathway.
Arterioscler Thromb Vasc Biol. 2014 May;34(5):985-95. doi: 10.1161/ATVBAHA.114.303415. Epub 2014 Mar 20.
6
MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1.
Nat Med. 2014 Apr;20(4):368-76. doi: 10.1038/nm.3487. Epub 2014 Mar 2.
7
Computational approaches for analyzing the mechanics of atherosclerotic plaques: a review.
J Biomech. 2014 Mar 3;47(4):859-69. doi: 10.1016/j.jbiomech.2014.01.011. Epub 2014 Jan 21.
8
Compensatory enlargement of the left main coronary artery: insights from the PROSPECT study.
Coron Artery Dis. 2014 Mar;25(2):98-103. doi: 10.1097/MCA.0000000000000074.
9
Inhibition of microRNA-92a prevents endothelial dysfunction and atherosclerosis in mice.
Circ Res. 2014 Jan 31;114(3):434-43. doi: 10.1161/CIRCRESAHA.114.302213. Epub 2013 Nov 19.
10
Urinary leukotriene E4 is associated with renal function but not with endothelial function in type 2 diabetes.
Dis Markers. 2013;35(5):475-80. doi: 10.1155/2013/370461. Epub 2013 Oct 2.

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

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验