Ontology highlight
ABSTRACT: Rationale
Atherosclerosis is, in part, caused by immune and inflammatory cell infiltration into the vascular wall, leading to enhanced inflammation and lipid accumulation in the aortic endothelium. Understanding the molecular mechanisms underlying this disease is critical for the development of new therapies. Our recent studies demonstrate that epsins, a family of ubiquitin-binding endocytic adaptors, are critical regulators of atherogenicity. Given the fundamental contribution lesion macrophages make to fuel atherosclerosis, whether and how myeloid-specific epsins promote atherogenesis is an open and significant question.Objective
We will determine the role of myeloid-specific epsins in regulating lesion macrophage function during atherosclerosis.Methods and results
SUBMITTER: Brophy ML
PROVIDER: S-EPMC6375743 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature