Figure 4 Acute-phase HDL Figure 4 | Acute-phase HDL. HDL undergoes substantial modification during an acute-phase response. Inflammatory cytokines induce the hepatic expression of acute-phase SAA and group IIa sPLA2, which leads to the formation of HDL particles that are relatively enriched in SAA and depleted of apoA-I and phospholipid. Increased oxidative stress during inflammation generates HDL that contains oxidatively modified apoA-I. In addition, HDL remodelling during inflammation generates an abundance of triglycerides and a loss of HDL-associated proteins such as apoA-II, CETP, LCAT, PAF-AH, and PON. Results from studies investigating the effect of inflammation on steps in the reverse cholesterol transport pathway have been conflicting. During inflammation, cellular cholesterol efflux by ABCA1 and ABCG1 might be unchanged, decreased, or increased, and the uptake by SCARB1 of CEs from acute-phase HDL into the liver for subsequent excretion is either decreased or unchanged. Abbreviations: ABCA1, ATP-binding cassette transporter A1; ABCG1, ATP-binding cassette transporter G1; apoA, apolipoprotein A; CE, cholesteryl ester; CETP, cholesterol ester transfer protein; HDL, high-density lipoprotein; LCAT, lecithin–cholesterol acyltransferase; PAF-AH, platelet-activating factor acetylhydrolase; PON, paraoxonase; SAA, serum amyloid A; SCARB1, scavenger receptor class B member 1; sPLA2, secretory phospholipase A2; TG, triglyceride. Rosenson, R. S. et al. (2015) Dysfunctional HDL and atherosclerotic cardiovascular disease Nat. Rev. Cardiol. doi:10.1038/nrcardio.2015.124