The accumulated evidence that oxidative modification of LDL plays an important role in the
pathogenesis of atherosclerosis in animal models is very strong. The negative results in
recent clinical studies have caused many to conclude that LDL oxidation may not be
relevant in the human disease. Yet many of the lines of evidence that support the hypothesis
have been demonstrated to apply also in humans. In this review, we briefly summarize the
lines of evidence on which the hypothesis rests, its strengths, and its weaknesses.