SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg.

ABSTRACT:

Background

Atherosclerosis (AS) is a cardiovascular problem, which is featured by the accumulation of lipids in the intimal layer of the arterial wall and inflammatory reaction of immune cells. CCL17 is an inflammatory mediator associated with promoting AS. Nevertheless, the specific role of CCL17 and its upstream regulatory mechanisms in macrophage mediated inflammation and AS remain unclear.

Methods

An AS mice model was established by subjecting ApoE^-/- mice to a high-fat diet (HFD). Constructing an AS cell model by treating primary macrophages with oxidized low-density lipoprotein (ox LDL). Injecting shRNA wrapped by AAV virus into the tail vein of mice knocked down CCL17 and SENP3 in mice. Hematoxylin-eosin (HE) and oil red O staining were used to detect arter

SUBMITTER: Zhao X 

PROVIDER: S-EPMC12634754 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature