MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities
Coronary artery disease (CAD) as part of the cardiovascular diseases is a pathology caused by atherosclerosis, a chronic inflammatory disease of the vessel wall characterized by a massive invasion of lipids and inflammatory cells into the inner vessel layer (intima) leading to the formation of ather...
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pubmed-45089252015-08-07 MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities van der Vorst, Emiel P. C. Döring, Yvonne Weber, Christian Immunology Coronary artery disease (CAD) as part of the cardiovascular diseases is a pathology caused by atherosclerosis, a chronic inflammatory disease of the vessel wall characterized by a massive invasion of lipids and inflammatory cells into the inner vessel layer (intima) leading to the formation of atherosclerotic lesions; their constant growth may cause complications such as flow-limiting stenosis and plaque rupture, the latter triggering vessel occlusion through thrombus formation. Pathophysiology of CAD is complex and over the last years many players have entered the picture. One of the latter being chemokines (small 8–12 kDa cytokines) and their receptors, known to orchestrate cell chemotaxis and arrest. Here, we will focus on the chemokine CXCL12, also known as stromal cell-derived factor 1 (SDF-1) and the chemokine-like function chemokine, macrophage migration-inhibitory factor (MIF). Both are ubiquitously expressed and highly conserved proteins and play an important role in cell homeostasis, recruitment, and arrest through binding to their corresponding chemokine receptors CXCR4 (CXCL12 and MIF), ACKR3 (CXCL12), and CXCR2 (MIF). In addition, MIF also binds to the receptor CD44 and the co-receptor CD74. CXCL12 has mostly been studied for its crucial role in the homing of (hematopoietic) progenitor cells in the bone marrow and their mobilization into the periphery. In contrast to CXCL12, MIF is secreted in response to diverse inflammatory stimuli, and has been associated with a clear pro-inflammatory and pro-atherogenic role in multiple studies of patients and animal models. Ongoing research on CXCL12 points at a protective function of this chemokine in atherosclerotic lesion development. This review will focus on the role of CXCL12 and MIF and their differences and similarities in CAD of high risk patients. Frontiers Media S.A. 2015-07-21 /pmc/articles/PMC4508925/ /pubmed/26257740 http://dx.doi.org/10.3389/fimmu.2015.00373 Text en Copyright © 2015 van der Vorst, Döring and Weber. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
van der Vorst, Emiel P. C. Döring, Yvonne Weber, Christian |
spellingShingle |
van der Vorst, Emiel P. C. Döring, Yvonne Weber, Christian MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
author_facet |
van der Vorst, Emiel P. C. Döring, Yvonne Weber, Christian |
author_sort |
van der Vorst, Emiel P. C. |
title |
MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
title_short |
MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
title_full |
MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
title_fullStr |
MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
title_full_unstemmed |
MIF and CXCL12 in Cardiovascular Diseases: Functional Differences and Similarities |
title_sort |
mif and cxcl12 in cardiovascular diseases: functional differences and similarities |
description |
Coronary artery disease (CAD) as part of the cardiovascular diseases is a pathology caused by atherosclerosis, a chronic inflammatory disease of the vessel wall characterized by a massive invasion of lipids and inflammatory cells into the inner vessel layer (intima) leading to the formation of atherosclerotic lesions; their constant growth may cause complications such as flow-limiting stenosis and plaque rupture, the latter triggering vessel occlusion through thrombus formation. Pathophysiology of CAD is complex and over the last years many players have entered the picture. One of the latter being chemokines (small 8–12 kDa cytokines) and their receptors, known to orchestrate cell chemotaxis and arrest. Here, we will focus on the chemokine CXCL12, also known as stromal cell-derived factor 1 (SDF-1) and the chemokine-like function chemokine, macrophage migration-inhibitory factor (MIF). Both are ubiquitously expressed and highly conserved proteins and play an important role in cell homeostasis, recruitment, and arrest through binding to their corresponding chemokine receptors CXCR4 (CXCL12 and MIF), ACKR3 (CXCL12), and CXCR2 (MIF). In addition, MIF also binds to the receptor CD44 and the co-receptor CD74. CXCL12 has mostly been studied for its crucial role in the homing of (hematopoietic) progenitor cells in the bone marrow and their mobilization into the periphery. In contrast to CXCL12, MIF is secreted in response to diverse inflammatory stimuli, and has been associated with a clear pro-inflammatory and pro-atherogenic role in multiple studies of patients and animal models. Ongoing research on CXCL12 points at a protective function of this chemokine in atherosclerotic lesion development. This review will focus on the role of CXCL12 and MIF and their differences and similarities in CAD of high risk patients. |
publisher |
Frontiers Media S.A. |
publishDate |
2015 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508925/ |
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1613250026215047168 |