» Articles » PMID: 26175090

Chemokines and Their Receptors in Atherosclerosis

Overview
Specialty General Medicine
Date 2015 Jul 16
PMID 26175090
Citations 45
Authors
Affiliations
Soon will be listed here.
Abstract

Atherosclerosis, a chronic inflammatory disease of the medium- and large-sized arteries, is the main underlying cause of cardiovascular diseases (CVDs) most often leading to a myocardial infarction or stroke. However, atherosclerosis can also develop without this clinical manifestation. The pathophysiology of atherosclerosis is very complex and consists of many cells and molecules interacting with each other. Over the last years, chemokines (small 8-12 kDa cytokines with chemotactic properties) have been identified as key players in atherogenesis. However, this remains a very active and dynamic field of research. Here, we will give an overview of the current knowledge about the involvement of chemokines in all phases of atherosclerotic lesion development. Furthermore, we will focus on two chemokines that recently have been associated with atherogenesis, CXCL12, and macrophage migration inhibitory factor (MIF). Both chemokines play a crucial role in leukocyte recruitment and arrest, a critical step in atherosclerosis development. MIF has shown to be a more pro-inflammatory and thus pro-atherogenic chemokine, instead CXCL12 seems to have a more protective function. However, results about this protective role are still quite debatable. Future research will further elucidate the precise role of these chemokines in atherosclerosis and determine the potential of chemokine-based therapies.

Citing Articles

The Role of Macrophage Inhibitory Factor in TAA-Induced Liver Fibrosis in Mice: Modulatory Effects of Betaine.

Radosavljevic T, Vukicevic D, Djuretic J, Gopcevic K, Labudovic Borovic M, Stankovic S Biomedicines. 2024; 12(6).

PMID: 38927544 PMC: 11201963. DOI: 10.3390/biomedicines12061337.


Inhibitory Effects of Simvastatin on IL-33-Induced MCP-1 via the Suppression of the JNK Pathway in Human Vascular Endothelial Cells.

Umebashi K, Yamamoto M, Tokito A, Sudou K, Takenoshita Y, Jougasaki M Int J Mol Sci. 2023; 24(16).

PMID: 37629196 PMC: 10456058. DOI: 10.3390/ijms241613015.


The Role of Punicalagin and Its Metabolites in Atherosclerosis and Risk Factors Associated with the Disease.

Alalawi S, Albalawi F, Ramji D Int J Mol Sci. 2023; 24(10).

PMID: 37239823 PMC: 10218101. DOI: 10.3390/ijms24108476.


Melatonin and TGF-β-Mediated Release of Extracellular Vesicles.

Piekarska K, Bonowicz K, Grzanka A, Jaworski L, Reiter R, Slominski A Metabolites. 2023; 13(4).

PMID: 37110233 PMC: 10142249. DOI: 10.3390/metabo13040575.


Rosuvastatin Attenuates Progression of Atherosclerosis and Reduces Serum IL6 and CCL2 Levels in Apolipoprotein-E-deficient Mice.

Tsilimigras D, Thanopoulou K, Salagianni M, Siasos G, Oikonomou E, Perrea D In Vivo. 2023; 37(3):994-1002.

PMID: 37103114 PMC: 10188013. DOI: 10.21873/invivo.13173.


References
1.
Sun J, Hartvigsen K, Chou M, Zhang Y, Sukhova G, Zhang J . Deficiency of antigen-presenting cell invariant chain reduces atherosclerosis in mice. Circulation. 2010; 122(8):808-20. PMC: 2927799. DOI: 10.1161/CIRCULATIONAHA.109.891887. View

2.
Feig J, Rong J, Shamir R, Sanson M, Vengrenyuk Y, Liu J . HDL promotes rapid atherosclerosis regression in mice and alters inflammatory properties of plaque monocyte-derived cells. Proc Natl Acad Sci U S A. 2011; 108(17):7166-71. PMC: 3084076. DOI: 10.1073/pnas.1016086108. View

3.
Stellos K, Bigalke B, Langer H, Geisler T, Schad A, Kogel A . Expression of stromal-cell-derived factor-1 on circulating platelets is increased in patients with acute coronary syndrome and correlates with the number of CD34+ progenitor cells. Eur Heart J. 2008; 30(5):584-93. DOI: 10.1093/eurheartj/ehn566. View

4.
Farouk S, Rader D, Reilly M, Mehta N . CXCL12: a new player in coronary disease identified through human genetics. Trends Cardiovasc Med. 2011; 20(6):204-9. PMC: 3235407. DOI: 10.1016/j.tcm.2011.08.002. View

5.
Maxfield F, Tabas I . Role of cholesterol and lipid organization in disease. Nature. 2005; 438(7068):612-21. DOI: 10.1038/nature04399. View