The central roles played by lipoproteins in atherosclerosis are well established. Increased plasma concentrations of low-density lipoproteins (LDLs) and triglyceride-rich remnant lipoproteins are highly atherogenic, whereas high-density lipoproteins (HDLs) are known to protect against lesion development. These effects are driven, in part, by the impact of these lipoproteins on inflammation-a process that is central to atherogenesis. In individuals with dyslipidaemia, LDLs and other atherogenic lipoproteins enter the arterial wall where they undergo chemical modification, including oxidation. These modified lipoproteins initiate the inflammatory process that culminates in atherosclerosis lesion development. The inflammation can be reversed by HDLs via several mechanisms. These include promotion of cholesterol efflux, inhibition of LDL oxidation and reduction of adhesion molecule expression. Recent work has shown that HDLs are also able to inhibit acute vascular inflammation. Given the central roles played by lipoproteins and inflammation in atherogenesis, effective anti-atherosclerotic treatments should both modify the lipid profile and target the ongoing inflammation. These criteria are fulfilled by statins, which reduce inflammation by both lipid-dependent and -independent mechanisms. Additional protection from atherosclerosis may be provided by novel therapies that aim to increase plasma levels and activity of HDLs.