Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jun;74(12):2263-2282.
doi: 10.1007/s00018-017-2490-4. Epub 2017 Feb 28.

Integrin signaling in atherosclerosis

Alexandra C Finney  1 , Karen Y Stokes  2 , Christopher B Pattillo  2 , A Wayne Orr  3   4   5
Affiliations
Review

Integrin signaling in atherosclerosis

Alexandra C Finney et al. Cell Mol Life Sci. 2017 Jun.

Abstract

Atherosclerosis, a chronic lipid-driven inflammatory disease affecting large arteries, represents the primary cause of cardiovascular disease in the world. The local remodeling of the vessel intima during atherosclerosis involves the modulation of vascular cell phenotype, alteration of cell migration and proliferation, and propagation of local extracellular matrix remodeling. All of these responses represent targets of the integrin family of cell adhesion receptors. As such, alterations in integrin signaling affect multiple aspects of atherosclerosis, from the earliest induction of inflammation to the development of advanced fibrotic plaques. Integrin signaling has been shown to regulate endothelial phenotype, facilitate leukocyte homing, affect leukocyte function, and drive smooth muscle fibroproliferative remodeling. In addition, integrin signaling in platelets contributes to the thrombotic complications that typically drive the clinical manifestation of cardiovascular disease. In this review, we examine the current literature on integrin regulation of atherosclerotic plaque development and the suitability of integrins as potential therapeutic targets to limit cardiovascular disease and its complications.

Keywords: Atherosclerosis; Extracellular matrix; Inflammation; Integrins; Migration; Proliferation.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Model for atherosclerotic plaque development. Progression of atherosclerotic plaques from alterations in early endothelial function to the progressive accumulation of macrophages and smooth muscle cells are shown. Intraplaque angiogenesis in large atherosclerotic lesions provide additional access sites for leukocyte targeting
Fig. 2
Fig. 2
Vascular integrin signaling. a The 24 mammalian integrin dimers are shown. Shading indicates their ligand binding specificity for collagen (blue), laminin (purple), or RGD motif-containing proteins (red), or their leukocyte-specific expression pattern (green). b Structure of integrin signaling complexes with their signaling, force transduction, and actin coupling layers
See this image and copyright information in PMC

References

    1. Kingsley K, et al. ERK1/2 mediates PDGF-BB stimulated vascular smooth muscle cell proliferation and migration on laminin-5. Biochem Biophys Res Commun. 2002;293(3):1000–1006. doi: 10.1016/S0006-291X(02)00331-5. - DOI - PubMed
    1. Chahine MN, et al. Oxidized LDL affects smooth muscle cell growth through MAPK-mediated actions on nuclear protein import. J Mol Cell Cardiol. 2009;46(3):431–441. doi: 10.1016/j.yjmcc.2008.10.009. - DOI - PubMed
    1. Orr AW, et al. Molecular mechanisms of collagen isotype-specific modulation of smooth muscle cell phenotype. Arterioscler Thromb Vasc Biol. 2009;29(2):225–231. doi: 10.1161/ATVBAHA.108.178749. - DOI - PMC - PubMed
    1. Autieri MV. Pro- and anti-inflammatory cytokine networks in atherosclerosis. ISRN Vasc Med. 2012;2012:17.
    1. Owens GK, Kumar MS, Wamhoff BR. Molecular regulation of vascular smooth muscle cell differentiation in development and disease. Physiol Rev. 2004;84(3):767–801. doi: 10.1152/physrev.00041.2003. - DOI - PubMed

Publication types