Key result
CEACAM1 deficiency cuts atherosclerotic plaque size by >50% in hyperlipidemic mice.
Why the study?
Does CEACAM1 deficiency reduce atherosclerotic plaque progression in Ldlr -/- mice?
Does CEACAM1 deficiency reduce atherosclerotic plaque progression in Ldlr -/- mice?
CEACAM1 deficiency reduces atherosclerotic plaque size by over 50% in a mouse model, suggesting it as a potential therapeutic target for atherosclerosis.
Introduction/Background: Atherosclerosis-related cardiovascular diseases are the leading cause of morbidity and mortality worldwide. The carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1, Cc1 ) plays a dual role in vascular biology, supporting early vascular development while fostering chronic inflammation in aging vasculature. Research Question/Hypothesis: Given the pro-inflammatory role of CEACAM1 in vascular aging, we hypothesized that CEACAM1 contributes to the progression of atherosclerosis. We therefore investigated its impact on atherosclerotic plaque development. Goals/Aims: This study aimed to define the role of CEACAM1 in atherogenesis using in vivo and in vitro models. Methods/Approach: Atherosclerotic plaque burden was analyzed in Ldlr -/- and Ldlr -/- / Cc1 -/- mice fed a high-fat diet. RNA sequencing of aortic arches was performed to identify differentially regulated signaling pathways. In vitro WT and Cc1 -/- EA.hy926 endothelial cells were analyzed for TNF-α/NF-κB activation, adhesion molecule expression, monocyte adhesion, endothelial permeability and LDL transcytosis. Results/Data: Ldlr -/- / Cc1 -/- mice exhibited a more than 50% reduction in atherosclerotic plaque size compared to Ldlr -/- controls. RNA sequencing revealed that CEACAM1 deficiency led to downregulation of TNF-α/NF-κB signaling, reduced adhesion molecule expression and impaired LDL uptake. Accordingly, in vitro Cc1 -/- endothelial cells showed attenuated TNF-α/NF-κB activation, decreased monocyte adhesion and reduced LDL transcytosis compared to WT controls. Conclusion: CEACAM1 emerges as a key regulator of atherosclerotic plaque progression by amplifying pro-inflammatory and lipid transport pathways. Therefore, CEACAM1 represents a potential therapeutic target to mitigate atherosclerosis-related cardiovascular complications.
No takes yet. Share an insight, caveat, or question.
Goetz et al. (2025) studied Atherosclerosis. CEACAM1 deficiency vs. Ldlr -/- controls was evaluated on Atherosclerotic plaque size. CEACAM1 deficiency reduced atherosclerotic plaque size by more than 50% in Ldlr -/- mice compared to controls.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: