| Increasing evidence suggests that myriad factors, including triglyceride-rich lipoproteins, endothelial cell apoptosis, increased monolayer permeability, TGF-beta1 and ATF3 all play a role in the development of atherosclerotic cardiovascular disease. The link between these phenomena and how they contribute to lesion development has not been explored. The goal of the present study was to determine whether TGRL lipolysis products may activate the TGF-beta1/Smad signaling cascade to induce ATF3 and initiate an apoptotic response in endothelial cells, which, via caspase-3, may alter junctional proteins to increase paracellular permeability and promote lesion formation. |
