Atherosclerotic progression at sites of low shear stress is attenuated by myeloid-PlexinD1 deficiency through suppression of classical macrophage polarization
Authors' conclusion
OSS drives atherosclerotic progression by suppressing endothelial PTGS2/PGE2 to promote PlexinD1/NF-κB-mediated M1 macrophage polarization.
Study context
- Population
- Patients with acute coronary syndrome (ACS) (plasma PlexinD1), human carotid plaques, and ApoE-deficient mice on high-fat, high-cholesterol diet
- Participants
- 72 ACS patients
- Comparison
- Myeloid-PlexinD1 knockout vs control in atherosclerotic mice; Oscillatory shear stress (OSS) vs LSS plaque sites
- Outcome
- Plasma PlexinD1, carotid bifurcation (OSS) vs common carotid (LSS) plaque features, and atherosclerotic lesions in myeloid-PlexinD1 knockout mice
Main finding
As reported in the abstract
Plasma PlexinD1 in ACS patients with vs without coronary bifurcation lesions
1.32-fold higher
Original publication
Atherosclerotic progression at sites of low shear stress is attenuated by myeloid-PlexinD1 deficiency through suppression of classical macrophage polarization. Eur Heart J. Published 17 December 2025. doi:10.
Summarised from the published abstract; every number is checked against it