Eva Xepapadaki, Christina Kalogeropoulou, Evangelia Zvintzou, Serafoula Filou, Kyriakos Kypreos
Abstract
Atherosclerosis is a multistep process that progresses over a long period of time and displays a broad range of severity. In its final form, it manifests as a lesion of the intimal layer of the arterial wall. Multiple epidemiological and clinical studies in the past suggested that reduced HDL cholesterol (HDL-C) levels may correlate with increased risk for atherosclerosis. More recent data indicated that high density lipoprotein (HDL) particle functionality rather than HDL-C levels is a much more important parameter for human health and disease. Recent data from clinical paradigms and studies in mice support the interesting hypothesis that variations in HDL proteome may set the basis for its functionality. Apolipoprotein A2 (APOA2) is the second most abundant protein of HDL and plays a crucial role in HDL particle synthesis. Studies in mice suggested a proatherogenic role for APOA2 though studies in humans failed thus far to establish a clear role for APOA2 in atherosclerosis. Interestingly, though APOA2 increases HDL-C levels, the effects of this protein on HDL functionality are not adequately investigated. Understanding how APOA2 affects HDL and the lipoprotein transport system may provide another important piece in the puzzle of the mechanisms linking plasma lipoproteins with atherosclerosis.
Keywords: High density lipoprotein, Atherosclerosis, Apolipoprotein A2