Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury

Abstract

Our understanding of the molecular signaling pathways regulating the initiation and progression of atherosclerosis or remodeling in response to injury has begun to cross the boundaries from regulation of well-described canonical pathways to the interplay between these pathways. The focus of this review is to summarize our current understanding of a finite group of transcription factors and kinases involved in vascular injury and atherosclerosis, including nuclear factor-kappaB (NF-kappaB), early growth response factor-1 (Egr-1), activator protein-1 (AP-1), hypoxia inducible factor-1alpha (HIF-1alpha), homeobox, and T cell factor/lymphoid enhancer factor (Tcf-Lef), as well as the kinases janus kinase/signal transducers and activators of transcription (JAK/STAT), protein kinase C (PKC), p38, Rho, ERK5, JNK, p44/p42, and phosphoinositide 3 (PI3) kinase/AKT.