More Cellular Signals for Atherogenesis?
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The potential importance of the nuclear factor κB (NF-κB) system as a key player in control of transcription of genes for mediators of a variety of inflammatory responses, from those mediated by cytokine pathways to atherogenesis and thrombogenesis, has been a topic of broad interest. The proteins of the NF-κB family that form the inactive heterodimeric complexes in the cytoplasm of cells, the inhibitors that prevent nuclear translocation, and the stimuli that lead to release and nuclear translocation of the active uninhibited NF-κB complexes, commonly referred to as activation, have received great attention, as have the many genes subject to transcriptional activation by the various heterodimeric NF-κB complexes once translocated to the nucleus. These details are central to the goal of mapping the cellular and molecular pathways of vascular injury, including atherosclerosis, restenosis, and other vascular pathobiology. The overall schema is growing richer in detail and interpretive hypotheses. However, the answers remain elusive. A valid schema is nevertheless critically important to discovery of molecular strategies for effective and safe intervention in acute and chronic diseases of the vasculature.
In the present issue of Circulation, Gawaz and colleagues1 advance our understanding of a cellular and molecular scenario most likely operative in the vascular pathology early in the atherogenic cascade and perhaps pertaining as well to the local activation of …