PuSH - Publication Server of Helmholtz Zentrum München

O'Connor, T. ; Borsig, L.* ; Heikenwälder, M.

CCL2-CCR2 signaling in disease pathogenesis.

Endocr. Metab. Immune Disord. Drug Targets 15, 105-118 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
The role of chemokines and their receptors in controlling several physiological and pathological processes has only become evident in the last couple of years. From a sole function of chemo-attraction, our view on chemokine receptor activation has switched to the regulation of pleiotropic signaling pathways influencing numerous molecular and cellular processes. The large number of chemokines and receptors and hence possible combinations of chemokine-chemokine receptor interactions, as well as the expression profiles of chemokines and chemokine receptors within particular cell types, has contributed to the complexity of chemokine receptor signaling as we see it today. The chemokine CCL2 and its main chemokine receptor CCR2 have been implicated in the pathogenesis of several different disease processes, including vascular permeability and attraction of immune cells during metastasis, a number of different neurological disorders, autoimmune disease, obesity, and atherosclerosis. Here we review recent findings on the role of the CCL2-CCR2 axis in the regulation of these diseases. We believe that research has only gained a first glimpse of what chemokines can control and what the underlying mechanisms are. There is certainly more to be found that will - with high certainty - have strong implications for clinical applications in the near future.
Altmetric
Additional Metrics?
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
Keywords Autoimmune Disease ; Cancer ; Ccl2 ; Ccr2 ; Chemokine ; Cns ; Mcp-1 ; Metastasis; Monocyte Chemoattractant Protein-1; Experimental Autoimmune Encephalomyelitis; Amyotrophic-lateral-sclerosis; Chemokine Receptor Ccr2; Central-nervous-system; Microvascular Endothelial-cells; Focal Cerebral-ischemia; Necrosis-factor-alpha; Neonatal-rat-brain; Hippocampal Slice Cultures
ISSN (print) / ISBN 1871-5303
Quellenangaben Volume: 15, Issue: 2, Pages: 105-118 Article Number: , Supplement: ,
Publisher Bentham Science Publishers
Publishing Place Bentham Science Publ.
Reviewing status Peer reviewed