BACKGROUND Antagonism or deletion of the receptor (the TP) for the cyclooxygenase (COX) product thromboxane (Tx)A2, retards atherogenesis in apolipoprotein E knockout (ApoE KO) mice. Although inhibition or deletion of COX-1 retards atherogenesis in ApoE and LDL receptor (LDLR) KOs, the role of COX-2 in atherogenesis remains controversial. Other products of COX-2, such as prostaglandin (PG) I2 a...

Chemical atherogenesis is an emerging field that describes how environmental pollutants and endogenous toxins perturb critical pathways that regulate lipid metabolism and inflammation, thus injuring cells found within the vessel wall. Despite growing awareness of the role of environmental pollutants in the development of cardiovascular disease, the field of chemical atherogenesis can broadly in...

An important early step in atherosclerosis is binding of apolipoprotein B-100 (apoB-100)– containing lipoproteins (VLDL, IDL, and LDL) to the proteoglycan component of the extracellular matrix of the arterial intima.1,2 When oxidative agents or enzymes attack the proteoglycan-bound lipoproteins, they become oxidatively modified, and when various intimal proteases or lipases hydrolyze them, they...

The potential importance of the nuclear factor kB (NF-kB) 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-kB family that form the inactive heterodimeric complexes in the cytoplasm of cells, the ...