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TAM 受体与心血管疾病。

TAM receptors in cardiovascular disease.

机构信息

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Sir Graeme Davies Building, 120 University Place, Glasgow, UK.

Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.

出版信息

Cardiovasc Res. 2019 Jul 1;115(8):1286-1295. doi: 10.1093/cvr/cvz100.

DOI:10.1093/cvr/cvz100
PMID:30980657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6587925/
Abstract

The TAM receptors are a distinct family of three receptor tyrosine kinases, namely Tyro3, Axl, and MerTK. Since their discovery in the early 1990s, they have been studied for their ability to influence numerous diseases, including cancer, chronic inflammatory and autoimmune disorders, and cardiovascular diseases. The TAM receptors demonstrate an ability to influence multiple aspects of cardiovascular pathology via their diverse effects on cells of both the vasculature and the immune system. In this review, we will explore the various functions of the TAM receptors and how they influence cardiovascular disease through regulation of vascular remodelling, efferocytosis and inflammation. Based on this information, we will suggest areas in which further research is required and identify potential targets for therapeutic intervention.

摘要

TAM 受体是一组独特的三种受体酪氨酸激酶家族,分别为 Tyro3、Axl 和 MerTK。自 20 世纪 90 年代初发现以来,它们一直因其影响多种疾病的能力而受到研究,包括癌症、慢性炎症和自身免疫性疾病以及心血管疾病。TAM 受体通过对血管和免疫系统细胞的多种作用,显示出影响心血管病理学多个方面的能力。在这篇综述中,我们将探讨 TAM 受体的各种功能,以及它们如何通过调节血管重塑、细胞吞噬作用和炎症来影响心血管疾病。基于这些信息,我们将提出需要进一步研究的领域,并确定潜在的治疗干预靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de2/6587925/840031df7cac/cvz100f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de2/6587925/c33726e46e46/cvz100f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de2/6587925/840031df7cac/cvz100f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de2/6587925/c33726e46e46/cvz100f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de2/6587925/840031df7cac/cvz100f2.jpg

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本文引用的文献

1
Regulatory T Cells Promote Macrophage Efferocytosis during Inflammation Resolution.调节性 T 细胞促进炎症消退期巨噬细胞的胞葬作用。
Immunity. 2018 Oct 16;49(4):666-677.e6. doi: 10.1016/j.immuni.2018.07.015. Epub 2018 Oct 2.
2
MerTK signaling in macrophages promotes the synthesis of inflammation resolution mediators by suppressing CaMKII activity.MerTK 信号在巨噬细胞中通过抑制 CaMKII 活性促进炎症解决介质的合成。
Sci Signal. 2018 Sep 25;11(549):eaar3721. doi: 10.1126/scisignal.aar3721.
3
miR-34a Promotes Vascular Smooth Muscle Cell Calcification by Downregulating SIRT1 (Sirtuin 1) and Axl (AXL Receptor Tyrosine Kinase).
TAM受体及配体蛋白S和Gas6在动脉粥样硬化与心血管疾病中的作用
Int J Mol Sci. 2024 Nov 27;25(23):12736. doi: 10.3390/ijms252312736.
4
Bisphenol C Induces Cardiac Developmental Defects by Disrupting mA Homeostasis.双酚 C 通过破坏 mA 平衡引起心脏发育缺陷。
Environ Sci Technol. 2024 Oct 1;58(39):17259-17269. doi: 10.1021/acs.est.4c04373. Epub 2024 Aug 29.
5
Could Gas6/TAM Axis Provide Valuable Insights into the Pathogenesis of Systemic Sclerosis?Gas6/TAM轴能否为系统性硬化症的发病机制提供有价值的见解?
Curr Issues Mol Biol. 2024 Jul 15;46(7):7486-7504. doi: 10.3390/cimb46070444.
6
Crosstalk between epitranscriptomic and epigenomic modifications and its implication in human diseases.表观转录组学修饰和表观基因组学修饰之间的串扰及其在人类疾病中的意义。
Cell Genom. 2024 Aug 14;4(8):100605. doi: 10.1016/j.xgen.2024.100605. Epub 2024 Jul 8.
7
Mechanism of efferocytosis in atherosclerosis.动脉粥样硬化中胞葬作用的机制。
J Mol Med (Berl). 2024 Jul;102(7):831-840. doi: 10.1007/s00109-024-02439-3. Epub 2024 May 10.
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Hepatology. 2018 Jan;67(1):216-231. doi: 10.1002/hep.29478. Epub 2017 Nov 29.