PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
October 24, 2008Arteriosclerosis Thrombosis and Vascular Biology259 citationsOpen Access

Loss of SR-A and CD36 Activity Reduces Atherosclerotic Lesion Complexity Without Abrogating Foam Cell Formation in Hyperlipidemic Mice

View Full Paper
JMJennifer J. Manning-TobinKMKathryn J. MooreTSTracie A. Seimon

Key Points

  • This research aims to investigate the impact of SR-A and CD36 deletion on atherosclerotic lesions and foam cell formation in hyperlipidemic mice.
  • Targeted deletion of SR-A and CD36 in Apoe(-/-) mice.
  • Assessment of foam cell formation and atherosclerotic lesion progression.
  • Evaluation of necrotic lesions and lesional inflammation.
  • Loss of SR-A and CD36 did not prevent foam cell formation in Apoe(-/-) mice.
  • Atherosclerotic lesion area remained substantially unchanged despite deletions.
  • Reduction in progression to advanced necrotic lesions was observed, indicating enhanced plaque stability.

Abstract

Although targeted deletion of SR-A and CD36 does not abrogate macrophage foam cell formation or substantially reduce atherosclerotic lesion area in Apoe(-/-) mice, loss of these pathways does reduce progression to more advanced necrotic lesions. These data suggest that targeted inhibition of these pathways in vivo may reduce lesional inflammation and promote plaque stability.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Manning-Tobin et al. (2008) studied this question.

synapsesocial.com/papers/69dab6ef00ab073a27838fd4https://doi.org/10.1161/atvbaha.108.176644
Ask AI
Helpful
Bookmark
Share
View Full Paper