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动脉粥样硬化的转录组学研究:揭示斑块表型并克服方法学挑战。

Transcriptomic research in atherosclerosis: Unravelling plaque phenotype and overcoming methodological challenges.

作者信息

Sopić Miron, Karaduzovic-Hadziabdic Kanita, Kardassis Dimitris, Maegdefessel Lars, Martelli Fabio, Meerson Ari, Munjas Jelena, Niculescu Loredan S, Stoll Monika, Magni Paolo, Devaux Yvan

机构信息

Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Luxembourg Institute of Health, L-1445 Strassen, Luxembourg.

Cardiovascular Research Unit, Department of Population Health, Luxembourg Institute of Health, L-1445 Strassen, Luxembourg.

出版信息

J Mol Cell Cardiol Plus. 2023 Sep 12;6:100048. doi: 10.1016/j.jmccpl.2023.100048. eCollection 2023 Dec.

DOI:10.1016/j.jmccpl.2023.100048
PMID:39802625
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11708385/
Abstract

Atherosclerotic disease is a major cause of acute cardiovascular events. A deeper understanding of its underlying mechanisms will allow advancing personalized and patient-centered healthcare. Transcriptomic research has proven to be a powerful tool for unravelling the complex molecular pathways that drive atherosclerosis. However, low reproducibility of research findings and lack of standardization of procedures pose significant challenges in this field. In this review, we discuss how transcriptomic research can help in understanding the different phenotypes of the atherosclerotic plaque that contribute to the development and progression of atherosclerosis. We highlight the methodological challenges that need to be addressed to improve research outputs, and emphasize the importance of research protocols harmonization. We also discuss recent advances in transcriptomic research, including bulk or single-cell sequencing, and their added value in plaque phenotyping. Finally, we explore how integrated multiomics data and machine learning improve understanding of atherosclerosis and provide directions for future research.

摘要

动脉粥样硬化疾病是急性心血管事件的主要原因。对其潜在机制的更深入理解将有助于推进个性化和以患者为中心的医疗保健。转录组学研究已被证明是揭示驱动动脉粥样硬化的复杂分子途径的有力工具。然而,研究结果的低重现性和程序缺乏标准化给该领域带来了重大挑战。在本综述中,我们讨论转录组学研究如何有助于理解动脉粥样硬化斑块的不同表型,这些表型有助于动脉粥样硬化的发生和发展。我们强调了为提高研究产出需要解决的方法学挑战,并强调了研究方案协调统一的重要性。我们还讨论了转录组学研究的最新进展,包括批量或单细胞测序,以及它们在斑块表型分析中的附加价值。最后,我们探讨了整合多组学数据和机器学习如何增进对动脉粥样硬化的理解,并为未来研究提供方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/a1e12882a15a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/5aead33968d5/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/87e71a4d836f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/21193150aa14/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/a1e12882a15a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/5aead33968d5/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/87e71a4d836f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/21193150aa14/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/308d/11708385/a1e12882a15a/gr3.jpg

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本文引用的文献

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Front Mol Med. 2022 Feb 22;2:839338. doi: 10.3389/fmmed.2022.839338. eCollection 2022.
2
Transcriptomic-based clustering of human atherosclerotic plaques identifies subgroups with different underlying biology and clinical presentation.基于转录组学的人类动脉粥样硬化斑块聚类可识别出具有不同潜在生物学特性和临床表现的亚组。
Nat Cardiovasc Res. 2022 Dec;1(12):1140-1155. doi: 10.1038/s44161-022-00171-0. Epub 2022 Dec 12.
3
New Biological Therapies for Low-Density Lipoprotein Cholesterol.
低密度脂蛋白胆固醇的新型生物疗法
Can J Cardiol. 2023 Dec;39(12):1913-1930. doi: 10.1016/j.cjca.2023.08.003. Epub 2023 Aug 9.
4
Spatial Transcriptional Mapping Reveals Site-Specific Pathways Underlying Human Atherosclerotic Plaque Rupture.空间转录组图谱揭示了人类动脉粥样硬化斑块破裂的特定部位相关途径。
J Am Coll Cardiol. 2023 Jun 13;81(23):2213-2227. doi: 10.1016/j.jacc.2023.04.008.
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The emerging landscape of non-conventional RNA functions in atherosclerosis.非典型 RNA 在动脉粥样硬化中的新兴功能领域。
Atherosclerosis. 2023 Jun;374:74-86. doi: 10.1016/j.atherosclerosis.2023.01.009. Epub 2023 Jan 20.
6
Long non-coding RNAs at the crossroad of vascular smooth muscle cell phenotypic modulation in atherosclerosis and neointimal formation.长链非编码 RNA 在动脉粥样硬化和血管平滑肌细胞表型调节及新生内膜形成中的作用。
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