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骨桥蛋白/分泌磷蛋白 1：免疫细胞与血管钙化之间的潜在介质。

Osteopontin/SPP1: a potential mediator between immune cells and vascular calcification.

机构信息

Department of Cardiovascular Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, China.

School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.

出版信息

Front Immunol. 2024 Jun 11;15:1395596. doi: 10.3389/fimmu.2024.1395596. eCollection 2024.

DOI:10.3389/fimmu.2024.1395596
PMID:38919629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11196619/
Abstract

Vascular calcification (VC) is considered a common pathological process in various vascular diseases. Accumulating studies have confirmed that VC is involved in the inflammatory response in heart disease, and SPP1+ macrophages play an important role in this process. In VC, studies have focused on the physiological and pathological functions of macrophages, such as pro-inflammatory or anti-inflammatory cytokines and pro-fibrotic vesicles. Additionally, macrophages and activated lymphocytes highly express SPP1 in atherosclerotic plaques, which promote the formation of fatty streaks and plaque development, and SPP1 is also involved in the calcification process of atherosclerotic plaques that results in heart failure, but the crosstalk between SPP1-mediated immune cells and VC has not been adequately addressed. In this review, we summarize the regulatory effect of SPP1 on VC in T cells, macrophages, and dendritic cells in different organs' VC, which could be a potential therapeutic target for VC.

摘要

血管钙化（VC）被认为是各种血管疾病中的一种常见病理过程。越来越多的研究证实，VC 参与了心脏病中的炎症反应，而 SPP1+巨噬细胞在这个过程中起着重要作用。在 VC 中，研究集中在巨噬细胞的生理和病理功能上，例如促炎或抗炎细胞因子和促纤维化小泡。此外，巨噬细胞和活化的淋巴细胞在动脉粥样硬化斑块中高度表达 SPP1，这促进了脂肪条纹的形成和斑块的发展，SPP1 也参与了导致心力衰竭的动脉粥样硬化斑块的钙化过程，但 SPP1 介导的免疫细胞与 VC 之间的串扰尚未得到充分解决。在这篇综述中，我们总结了 SPP1 在不同器官 VC 中的 T 细胞、巨噬细胞和树突状细胞中对 VC 的调节作用，这可能是 VC 的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac53/11196619/e36a6c5a193f/fimmu-15-1395596-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac53/11196619/23a618c3957f/fimmu-15-1395596-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac53/11196619/e36a6c5a193f/fimmu-15-1395596-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac53/11196619/23a618c3957f/fimmu-15-1395596-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac53/11196619/e36a6c5a193f/fimmu-15-1395596-g002.jpg

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本文引用的文献

[1]
Integrated bioinformatics analysis identified leucine rich repeat containing 15 and secreted phosphoprotein 1 as hub genes for calcific aortic valve disease and osteoarthritis.

IET Syst Biol. 2024-6

[2]
Coronary Artery Calcification: Current Concepts and Clinical Implications.

Circulation. 2024-1-16

[3]
Analysis of brain and blood single-cell transcriptomics in acute and subacute phases after experimental stroke.

Nat Immunol. 2024-2

[4]
Senescent skeletal muscle fibroadipogenic progenitors recruit and promote M2 polarization of macrophages.

Aging Cell. 2024-3

[5]
Pro-osteogenic role of interleukin-22 in calcific aortic valve disease.

Atherosclerosis. 2024-1

[6]
Isoforskolin modulates AQP4-SPP1-PIK3C3 related pathway for chronic obstructive pulmonary disease via cAMP signaling.

Chin Med. 2023-10-10

[7]
Bone-derived PDGF-BB drives brain vascular calcification in male mice.

J Clin Invest. 2023-12-1

[8]
Associations of cortical SPP1 and ITGAX with cognition and common neuropathologies in older adults.

Alzheimers Dement. 2024-1

[9]
Systems level identification of a matrisome-associated macrophage polarisation state in multi-organ fibrosis.

Elife. 2023-9-14

[10]
Calprotectin is a contributor to and potential therapeutic target for vascular calcification in chronic kidney disease.

Sci Transl Med. 2023-9-6

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