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主动脉瓣狭窄中的新型循环生物标志物

Novel Circulating Biomarkers in Aortic Valve Stenosis.

作者信息

Ong Joy Yi-Shan, Tan Sarah Ming Li, Koh Angela S, Kong William, Sia Ching Hui, Yeo Tiong Cheng, Quek Swee Chye, Poh Kian Keong

机构信息

Department of Cardiology, National University Heart Centre Singapore, Singapore 119074, Singapore.

National Heart Centre Singapore, Singapore 169609, Singapore.

出版信息

Int J Mol Sci. 2025 Feb 22;26(5):1902. doi: 10.3390/ijms26051902.


DOI:10.3390/ijms26051902
PMID:40076529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11899762/
Abstract

The underlying pathophysiology of aortic stenosis and factors affecting its clinical progression remain poorly understood. Apart from B-type natriuretic peptide (BNP), novel and emerging biomarkers have been described in association with aortic stenosis, emphasising the potential for these biomarkers to illuminate on yet unknown mechanisms of its pathogenesis. In this review, we aimed to summarise what is known about aortic stenosis biomarkers, highlight the emerging ones, and provide a roadmap for translating these insights into clinical applications. Among the biomarkers studied, lipoprotein(a) [Lp(a)] has emerged as the most promising for risk stratification. Elevated Lp(a) levels are often associated with more rapid aortic stenosis progression. This detrimental effect is attributed to its role in promoting valve calcification. While other emerging biomarkers such as matrix metalloproteinases, monocytes, and metabolites show promises, their specific roles in aortic stenosis pathophysiology remain less clear. This may be due to their relatively recent discovery. Ongoing research aims to elucidate their mechanisms of action.

摘要

主动脉瓣狭窄的潜在病理生理学以及影响其临床进展的因素仍未得到充分了解。除了B型利钠肽(BNP)外,还发现了一些与主动脉瓣狭窄相关的新型生物标志物,这凸显了这些生物标志物在阐明其发病机制中未知机制方面的潜力。在本综述中,我们旨在总结关于主动脉瓣狭窄生物标志物的已知信息,突出新兴的生物标志物,并提供将这些见解转化为临床应用的路线图。在研究的生物标志物中,脂蛋白(a)[Lp(a)]已成为风险分层最有前景的指标。Lp(a)水平升高通常与主动脉瓣狭窄进展更快有关。这种有害作用归因于其在促进瓣膜钙化中的作用。虽然其他新兴生物标志物如基质金属蛋白酶、单核细胞和代谢产物显示出前景,但其在主动脉瓣狭窄病理生理学中的具体作用仍不太清楚。这可能是由于它们相对较新才被发现。正在进行的研究旨在阐明其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9861/11899762/744ccadcaf01/ijms-26-01902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9861/11899762/744ccadcaf01/ijms-26-01902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9861/11899762/744ccadcaf01/ijms-26-01902-g001.jpg

相似文献

[1]
Novel Circulating Biomarkers in Aortic Valve Stenosis.

Int J Mol Sci. 2025-2-22

[2]
Role of lipoprotein (a) and LPA KIV2 repeat polymorphism in bicuspid aortic valve stenosis and calcification: a proof of concept study.

Intern Emerg Med. 2018-8-11

[3]
Lipoprotein(a) and Oxidized Phospholipids Promote Valve Calcification in Patients With Aortic Stenosis.

J Am Coll Cardiol. 2019-5-7

[4]
Oxidized Phospholipids, Lipoprotein(a), and Progression of Calcific Aortic Valve Stenosis.

J Am Coll Cardiol. 2015-9-15

[5]
Lipoprotein(a) and calcific aortic valve stenosis: A systematic review.

Prog Cardiovasc Dis. 2020-6-8

[6]
The influence of lipoprotein(a) on aortic valve calcification in patients undergoing transcatheter aortic valve replacement.

Clin Res Cardiol. 2025-3

[7]
What is the ultimate test that lowering lipoprotein(a) is beneficial for cardiovascular disease and aortic stenosis?

Curr Opin Lipidol. 2014-12

[8]
Comparison of Lipoprotein(a)-Levels in Patients ≥70 Years of Age With Versus Without Aortic Valve Stenosis.

Am J Cardiol. 2018-8-15

[9]
Association of Mild to Moderate Aortic Valve Stenosis Progression With Higher Lipoprotein(a) and Oxidized Phospholipid Levels: Secondary Analysis of a Randomized Clinical Trial.

JAMA Cardiol. 2018-12-1

[10]
Blood, tissue and imaging biomarkers in calcific aortic valve stenosis: past, present and future.

Curr Opin Cardiol. 2018-3

本文引用的文献

[1]
Association of Lipoprotein(a) With Severe Degenerative Aortic Valve Stenosis.

JACC Asia. 2024-9-10

[2]
Genetic causal association between lipidomic profiles, inflammatory proteomics, and aortic stenosis: a Mendelian randomization investigation.

Eur J Med Res. 2024-8-31

[3]
Human Aortic Stenotic Valve-Derived Extracellular Vesicles Induce Endothelial Dysfunction and Thrombogenicity Through AT1R/NADPH Oxidases/SGLT2 Pro-Oxidant Pathway.

JACC Basic Transl Sci. 2024-5-29

[4]
Lipoprotein(a) Levels in Disaggregated Racial and Ethnic Subgroups Across Atherosclerotic Cardiovascular Disease Risk Levels.

JACC Adv. 2024-5-2

[5]
Identifying People at High Risk for Severe Aortic Stenosis: Aortic Valve Calcium Versus Lipoprotein(a) and Low-Density Lipoprotein Cholesterol.

Circ Cardiovasc Imaging. 2024-6

[6]
Post-Procedure Monocyte Count Levels Predict Major Adverse Cardiovascular Events (MACE) Following Transcatheter Aortic Valve Implantation (TAVI) for Aortic Stenosis.

Heart Lung Circ. 2024-9

[7]
Discovery of potent small-molecule inhibitors of lipoprotein(a) formation.

Nature. 2024-5

[8]
Granzyme B degrades extracellular matrix and promotes inflammation and choroidal neovascularization.

Angiogenesis. 2024-8

[9]
New clinical trial design in precision medicine: discovery, development and direction.

Signal Transduct Target Ther. 2024-3-4

[10]
Large-Scale Proteomics Identifies Novel Biomarkers and Circulating Risk Factors for Aortic Stenosis.

J Am Coll Cardiol. 2024-2-6

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