Format:
Online-Ressource
Content:
Chronic low-grade inflammation drives atherosclerosis and despite optimal pharmacological treatment of classical cardiovascular risk factors, one third of the patients with atherosclerotic cardiovascular disease has elevated inflammatory biomarkers. Additional anti-inflammatory strategies to target this residual inflammatory cardiovascular risk are therefore required. T-cells are a dominant cell type in human atherosclerotic lesions. Modulation of T-cell activation is therefore a potential strategy to target inflammation in atherosclerosis. Ubiquitination is an important regulatory mechanism of T-cell activation and several E3 ubiquitin ligases, including casitas B-lineage lymphoma proto-oncogene B (Cbl-B), itchy homolog (Itch), and gene related to anergy in lymphocytes (GRAIL), function as a natural brake on T-cell activation. In this review we discuss recent insights on the role of Cbl-B, Itch, and GRAIL in atherosclerosis and explore the therapeutic potential of these E3 ubiquitin ligases in cardiovascular medicine.
In:
Datenlieferant: Open Access LMU (Ludwig-Maximilians-University Munich)
Language:
English
DOI:
10.3389/fcvm.2020.00106
URN:
urn:nbn:de:bvb:19-epub-88067-3
URL:
https://doi.org/10.3389/fcvm.2020.00106
URL:
https://nbn-resolving.org/urn:nbn:de:bvb:19-epub-88067-3
URL:
https://epub.ub.uni-muenchen.de/88067/1/fcvm-07-00106.pdf
URL:
https://epub.ub.uni-muenchen.de/88067/