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补体系统在血管钙化过程中的新认识。

New insight of complement system in the process of vascular calcification.

机构信息

Department of Cardiology, The Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.

State Key Laboratory for Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.

出版信息

J Cell Mol Med. 2023 May;27(9):1168-1178. doi: 10.1111/jcmm.17732. Epub 2023 Apr 1.


DOI:10.1111/jcmm.17732
PMID:37002701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10148053/
Abstract

The complement system defences against pathogenic microbes and modulates immune homeostasis by interacting with the innate and adaptive immune systems. Dysregulation, impairment or inadvertent activation of complement system contributes to the pathogenesis of some autoimmune diseases and cardiovascular diseases (CVD). Vascular calcification is the pivotal pathological basis of CVD, and contributes to the high morbidity and mortality of CVD. Increasing evidences indicate that the complement system plays a key role in chronic kidney diseases, atherosclerosis, diabetes mellitus and aging-related diseases, which are closely related with vascular calcification. However, the effect of complement system on vascular calcification is still unclear. In this review, we summarize current evidences about the activation of complement system in vascular calcification. We also describe the complex network of complement system and vascular smooth muscle cells osteogenic transdifferentiation, systemic inflammation, endoplasmic reticulum stress, extracellular matrix remodelling, oxidative stress, apoptosis in vascular calcification. Hence, providing a better understanding of the potential relationship between complement system and vascular calcification, so as to provide a direction for slowing the progression of this burgeoning health concern.

摘要

补体系统通过与先天和适应性免疫系统相互作用来防御致病微生物并调节免疫稳态。补体系统的失调、损伤或意外激活导致了一些自身免疫性疾病和心血管疾病 (CVD) 的发病机制。血管钙化是 CVD 的关键病理基础,导致 CVD 的高发病率和死亡率。越来越多的证据表明,补体系统在慢性肾脏病、动脉粥样硬化、糖尿病和与衰老相关的疾病中发挥着关键作用,这些疾病与血管钙化密切相关。然而,补体系统对血管钙化的影响仍不清楚。在这篇综述中,我们总结了补体系统在血管钙化中的激活的现有证据。我们还描述了补体系统与血管平滑肌细胞成骨转化、全身炎症、内质网应激、细胞外基质重塑、氧化应激、血管钙化中的细胞凋亡之间复杂的网络关系。因此,更好地了解补体系统与血管钙化之间的潜在关系,为减缓这一日益严重的健康问题的进展提供了方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0727/10148053/f417d326aaf3/JCMM-27-1168-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0727/10148053/4584c5977045/JCMM-27-1168-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0727/10148053/f417d326aaf3/JCMM-27-1168-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0727/10148053/4584c5977045/JCMM-27-1168-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0727/10148053/f417d326aaf3/JCMM-27-1168-g001.jpg

相似文献

[1]
New insight of complement system in the process of vascular calcification.

J Cell Mol Med. 2023-5

[2]
Impact of C-reactive protein on osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells.

Aging (Albany NY). 2019-8-3

[3]
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Kidney Int. 2014-3

[4]
Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms: Inhibition of Vascular Smooth Muscle Cell Osteogenic Conversion and Interaction With Collagen.

Arterioscler Thromb Vasc Biol. 2017-7

[5]
Breast arterial calcification in chronic kidney disease: absence of smooth muscle apoptosis and osteogenic transdifferentiation.

Kidney Int. 2013-9-18

[6]
[New mechanisms of chronic kidney disease-associated vascular calcification].

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[7]
Magnesium Counteracts Vascular Calcification: Passive Interference or Active Modulation?

Arterioscler Thromb Vasc Biol. 2017-8

[8]
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[9]
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[10]
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Kidney Int. 2014-10

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本文引用的文献

[1]
C5b-9 mediates ferroptosis of tubular epithelial cells in trichloroethylene-sensitization mice.

Ecotoxicol Environ Saf. 2022-10-1

[2]
The Complement System, Aging, and Aging-Related Diseases.

Int J Mol Sci. 2022-8-4

[3]
The Complement System in Metabolic-Associated Kidney Diseases.

Front Immunol. 2022

[4]
Overexpression of Decay Accelerating Factor Mitigates Fibrotic Responses to Lung Injury.

Am J Respir Cell Mol Biol. 2022-10

[5]
The multifaceted impact of complement on atherosclerosis.

Atherosclerosis. 2022-6

[6]
Complement factor B regulates cellular senescence and is associated with poor prognosis in pancreatic cancer.

Cell Oncol (Dordr). 2021-8

[7]
Saponins isolated from Radix polygalae extent lifespan by modulating complement C3 and gut microbiota.

Pharmacol Res. 2021-8

[8]
Oxidative stress in vascular calcification.

Clin Chim Acta. 2021-8

[9]
FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress.

Cell Death Dis. 2021-4-15

[10]
Antioxidant and C5a-blocking strategy for hepatic ischemia-reperfusion injury repair.

J Nanobiotechnology. 2021-4-15

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