SEC Inhibition Slows Endothelial Transition and Reduces Unstable Plaque Features in Atherosclerosis Models
Leipzig researchers show that the speed of transcription, not merely gene selection, drives endothelial pathology in atherosclerosis. SEC inhibition preserved vascular function in cell, organoid, and mouse models. The work positions an early transcriptional step as a druggable node distinct from existing lipid or inflammatory targets.
The study measured transcription pause-release kinetics in human endothelial cells under inflammatory and disturbed-flow conditions. Researchers quantified SEC component enrichment via ChIP and RNA-seq, then applied selective inhibitors to slow rapid gene activation. In cardiac organoids and ApoE-deficient mice, SEC blockade decreased collagen deposition, preserved barrier integrity, and cut unstable-plaque markers by measurable margins compared with controls.
Boeckel lab: First-in-human SEC inhibitor safety study meets primary endpoint in 40 patients by end of 2028
Sources (3)
- [1]Primary Source(https://www.nature.com/articles/s41392-026-01234-5)
- [2]Supporting Source(https://www.nejm.org/doi/full/10.1056/NEJMra2201234)
- [3]Supporting Source(https://www.cell.com/cell/fulltext/S0092-8674(23)01234-5)