English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Macrophage scavenger receptors (SRs), particularly type A SR (SR-A) and CD36, have been implicated in binding and internalizing modified forms of low-density lipoprotein (LDL) through a mechanism not regulated by cellular cholesterol content, resulting in cholesterol accumulation and foam cell formation. To test the impact of the absence of these receptors on lipid-mediated injuries in aortas or livers under inflammatory stress, C57BL/6 mice with knocked out SR-A and CD36 (SR DKO) were administered a combination of a high-fat diet and casein injection for 14 weeks. We analyzed the lipid accumulation in the aortas and livers, assessing lipid droplets, circulating inflammatory cytokines, serum lipid levels and gene expression of cholesterol uptake. Lipid accumulation in the aortas and livers of the inflammatory mice were assessed by morphologic and quantitative assay of cholesterol ester in the livers. The SR DKO mice under inflammatory stress showed an increased level of serum amyloid A, but did not exhibit any significantly increased levels of TNF-α and IL-6, while morphological analysis revealed a significant increase in lipid accumulation in the aortas and livers of the inflammatory mice. Although SR DKO mice exhibit substantially reduced inflammatory cytokine factors, loss of the SR pathway does accelerate lipid accumulation through LDL receptor pathways to lipid accumulation. These data suggest that targeted inhibition of SR pathways in vivo may promote lipid-mediated injuries in aortas and livers under inflammatory stress.

Inflammatory stress promotes lipid accumulation in the aorta and liver of SR-A/CD36 double knock-out mice