Atherosclerosis is characterized by chronic inflammation of an injured inti
ma. The pathological processes are initiated by accumulation of morphologic
ally distinct, modified forms of LDL, and followed by cellular infiltration
and foam cell formation. Activated intimal cells secrete enzymes and agent
s capable of modifying LDL, and the modified lipids of LDL, in turn, are ab
le to activate intimal cells and to trigger various inflammatory signals. T
hese processes can initiate and maintain a vicious circle in the intima and
lead to lesion progression. In this review, we focus on the LDL modificati
ons relevant to the initial lipid accumulation and discuss their pro-inflam
matory effects.