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COMP的降低可作为主动脉夹层进展预警的预测指标。

The Reduction of COMP Serves as a Predictor for Warning of Aortic Dissection Progression.

作者信息

Li Zhuofan, Gong Ze, Li Weihao, Chen Yanghui, Dai Rongbo, Yang Shiyu, Chen Yufei, Yu Fang, Fu Yi, Li Wei, Wang Dao Wen, Jia Yiting, Kong Wei

机构信息

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.

Hwamei College of Life and Health Sciences, Zhejiang Wanli University, Ningbo, China.

出版信息

JACC Basic Transl Sci. 2025 Jul 17;10(8):101329. doi: 10.1016/j.jacbts.2025.101329.

DOI:10.1016/j.jacbts.2025.101329
PMID:40680508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12296508/
Abstract

Thoracic aortic dissection (TAD) is a life-threatening cardiovascular disease that is associated with high morbidity and mortality. The prevailing challenge in TAD monitoring and diagnosis is the lack of novel biomarkers. A significant and sustained reduction in plasma cartilage oligomeric matrix protein (COMP) levels was observed through a case control analysis conducted in 362 TAD patients and 136 controls. The protective role of COMP was assessed in two TAD mouse models. These data suggested that a decreased plasma COMP level might serve as a novel biomarker for TAD progression and COMP could suppress the development of TAD and ameliorate vascular pathogenesis.

摘要

胸主动脉夹层(TAD)是一种危及生命的心血管疾病,具有高发病率和死亡率。TAD监测和诊断面临的主要挑战是缺乏新型生物标志物。通过对362例TAD患者和136例对照进行病例对照分析,观察到血浆软骨寡聚基质蛋白(COMP)水平显著且持续降低。在两种TAD小鼠模型中评估了COMP的保护作用。这些数据表明,血浆COMP水平降低可能作为TAD进展的新型生物标志物,并且COMP可以抑制TAD的发展并改善血管发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/a5a73b785c92/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/a4988a4b5113/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/54b5b77e7aaa/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/a5a73b785c92/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/a4988a4b5113/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/54b5b77e7aaa/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf6d/12296508/a5a73b785c92/gr5.jpg

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Ann Med. 2025 Dec;57(1):2478477. doi: 10.1080/07853890.2025.2478477. Epub 2025 Mar 21.
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Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.抑制主动脉CX3CR1+巨噬细胞可减轻小鼠马凡综合征胸主动脉瘤的进展。
J Clin Invest. 2025 Jan 16;135(2):e178198. doi: 10.1172/JCI178198.
3
Expression of , , and genes in aortic dissection.
、、和基因在主动脉夹层中的表达。
Exp Ther Med. 2024 Jul 10;28(3):360. doi: 10.3892/etm.2024.12649. eCollection 2024 Sep.
4
Marfan Syndrome: Enhanced Diagnostic Tools and Follow-up Management Strategies.马凡氏综合征:增强的诊断工具及随访管理策略
Diagnostics (Basel). 2023 Jul 5;13(13):2284. doi: 10.3390/diagnostics13132284.
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ADAMTS-7 deficiency attenuates thoracic aortic aneurysm and dissection in mice.ADAMTS - 7缺乏可减轻小鼠胸主动脉瘤和主动脉夹层的发生。
J Mol Med (Berl). 2023 Mar;101(3):237-248. doi: 10.1007/s00109-023-02284-w. Epub 2023 Jan 20.
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