TY - JOUR
T1 - Key Chemokine Pathways in Atherosclerosis and Their Therapeutic Potential
AU - Marquez, A.B.
AU - van der Vorst, E.P.C.
AU - Maas, S.L.
N1 - Funding Information:
This work is supported by a grant from the Interdisciplinary Center for Clinical Research within the Faculty of Medicine at the RWTH Aachen University, the DZHK (German Centre for Cardiovascular Research) and the BMBF (German Ministry of Education and Research), NWOZonMw Veni (91619053), the Else Kröner-Fresenius Stiftung (2018-A123) and the Fritz Thyssen Stiftung (10.20.2.043MN) to E.P.C.v.d.V.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/9/1
Y1 - 2021/9/1
N2 - The search to improve therapies to prevent or treat cardiovascular diseases (CVDs) rages on, as CVDs remain a leading cause of death worldwide. Here, the main cause of CVDs, atherosclerosis, and its prevention, take center stage. Chemokines and their receptors have long been known to play an important role in the pathophysiological development of atherosclerosis. Their role extends from the initiation to the progression, and even the potential regression of atherosclerotic lesions. These important regulators in atherosclerosis are therefore an obvious target in the development of therapeutic strategies. A plethora of preclinical studies have assessed various possibilities for targeting chemokine signaling via various approaches, including competitive ligands and microRNAs, which have shown promising results in ameliorating atherosclerosis. Developments in the field also include detailed imaging with tracers that target specific chemokine receptors. Lastly, clinical trials revealed the potential of various therapies but still require further investigation before commencing clinical use. Although there is still a lot to be learned and investigated, it is clear that chemokines and their receptors present attractive yet extremely complex therapeutic targets. Therefore, this review will serve to provide a general overview of the connection between various chemokines and their receptors with atherosclerosis. The different developments, including mouse models and clinical trials that tackle this complex interplay will also be explored.
AB - The search to improve therapies to prevent or treat cardiovascular diseases (CVDs) rages on, as CVDs remain a leading cause of death worldwide. Here, the main cause of CVDs, atherosclerosis, and its prevention, take center stage. Chemokines and their receptors have long been known to play an important role in the pathophysiological development of atherosclerosis. Their role extends from the initiation to the progression, and even the potential regression of atherosclerotic lesions. These important regulators in atherosclerosis are therefore an obvious target in the development of therapeutic strategies. A plethora of preclinical studies have assessed various possibilities for targeting chemokine signaling via various approaches, including competitive ligands and microRNAs, which have shown promising results in ameliorating atherosclerosis. Developments in the field also include detailed imaging with tracers that target specific chemokine receptors. Lastly, clinical trials revealed the potential of various therapies but still require further investigation before commencing clinical use. Although there is still a lot to be learned and investigated, it is clear that chemokines and their receptors present attractive yet extremely complex therapeutic targets. Therefore, this review will serve to provide a general overview of the connection between various chemokines and their receptors with atherosclerosis. The different developments, including mouse models and clinical trials that tackle this complex interplay will also be explored.
KW - chemokines
KW - chemokine receptors
KW - cardiovascular disease
KW - atherosclerosis
KW - RECEPTOR 4 EXPRESSION
KW - REDUCES ATHEROSCLEROSIS
KW - PLATELET CHEMOKINES
KW - PROMOTES ATHEROSCLEROSIS
KW - LIMITS ATHEROSCLEROSIS
KW - RHEUMATOID-ARTHRITIS
KW - PLAQUE-FORMATION
KW - LESION FORMATION
KW - DENDRITIC CELLS
KW - NUCLEAR-FACTOR
U2 - 10.3390/jcm10173825
DO - 10.3390/jcm10173825
M3 - (Systematic) Review article
C2 - 34501271
SN - 2077-0383
VL - 10
JO - Journal of Clinical Medicine
JF - Journal of Clinical Medicine
IS - 17
M1 - 3825
ER -