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[骨血管轴共病研究中动物模型的进展]

[Advances in Animal Modeling in the Study of Bone-Vascular Axis Comorbidities].

作者信息

Li Jiayang, Zhou Yumeng, Luo Yuwen, Huang Xuelin, Zhang Demao, Liu Xiaoheng

机构信息

( 610041) Institute of Biomedical Engineering, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2025 Mar 20;56(2):355-363. doi: 10.12182/20250360504.


DOI:10.12182/20250360504
PMID:40599294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12207050/
Abstract

Osteoporosis and cardiovascular calcification, two major age-related chronic diseases that China is confronting today, pose serious threats to public health. Previous studies have reported overlapping connections in the pathological processes and molecular mechanisms of these two diseases, particularly concerning inflammation, oxidative stress, and dysregulation of mineral metabolism, and that these two diseases tend to share common pathogenic factors. However, research exploring the comorbidity mechanisms of the two diseases remains limited in both depth and scope, largely due to the lack of widely accepted comorbidity animal models. Herein, we analyzed the latest research findings on the comorbidity mechanisms of vascular calcification and osteoporosis, focusing on summarizing the animal disease models currently in extensive use and the relevant evaluation criteria. We aim to provide new references for comorbidity research models and offer scientific evidence for future studies on pathological mechanisms and the development of new therapeutic strategies.

摘要

骨质疏松症和心血管钙化是中国目前面临的两种主要的与年龄相关的慢性疾病,对公众健康构成严重威胁。先前的研究报告了这两种疾病在病理过程和分子机制上存在重叠联系,特别是在炎症、氧化应激和矿物质代谢失调方面,并且这两种疾病往往具有共同的致病因素。然而,探索这两种疾病合并症机制的研究在深度和广度上仍然有限,这主要是由于缺乏广泛接受的合并症动物模型。在此,我们分析了血管钙化和骨质疏松症合并症机制的最新研究结果,重点总结了目前广泛使用的动物疾病模型及相关评估标准。我们旨在为合并症研究模型提供新的参考,并为未来关于病理机制的研究和新治疗策略的开发提供科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d5/12207050/001e78c5e404/scdxxbyxb-56-2-355-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d5/12207050/1406d644f50c/scdxxbyxb-56-2-355-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d5/12207050/001e78c5e404/scdxxbyxb-56-2-355-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d5/12207050/1406d644f50c/scdxxbyxb-56-2-355-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d5/12207050/001e78c5e404/scdxxbyxb-56-2-355-2.jpg

相似文献

[1]
[Advances in Animal Modeling in the Study of Bone-Vascular Axis Comorbidities].

Sichuan Da Xue Xue Bao Yi Xue Ban. 2025-3-20

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[7]
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本文引用的文献

[1]
GDF10 is a negative regulator of vascular calcification.

J Biol Chem. 2024-11

[2]
Interplay between bone marrow adiposity and bone resorption in RANKL-mediated modelled osteoporosis.

J Cell Physiol. 2024-12

[3]
The Importance of Vitamin K and the Combination of Vitamins K and D for Calcium Metabolism and Bone Health: A Review.

Nutrients. 2024-7-25

[4]
Augmentative effects of leukemia inhibitory factor reveal a critical role for TYK2 signaling in vascular calcification.

Kidney Int. 2024-10

[5]
Orphan Nuclear Receptor NR4A3 Promotes Vascular Calcification via Histone Lactylation.

Circ Res. 2024-5-24

[6]
Novel Biomarkers of Bone Metabolism.

Nutrients. 2024-2-22

[7]
Carbonylation of Runx2 at K176 by 4-Hydroxynonenal Accelerates Vascular Calcification.

Circulation. 2024-5-28

[8]
Heterogeneous osteoimmune profiles via single-cell transcriptomics in osteoporotic patients who fail bisphosphonate treatment.

Proc Natl Acad Sci U S A. 2024-2-20

[9]
The Bone-Vascular Axis in Chronic Kidney Disease: From Pathophysiology to Treatment.

Curr Osteoporos Rep. 2024-2

[10]
Early aging and premature vascular aging in chronic kidney disease.

Clin Kidney J. 2023-4-6

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