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This suppression is independent of plasma cholesterol changes and BW reduction through regulating markers of plaque instability and inflammation including those linked to plaque hemorrhage (CD163), matrix turnover (matrix metalloproteinase (MMP)-3, MMP-13), cholesterol metabolism (prostaglandin I2 synthase (PTGIS), ATP-binding cassette transporter 1 (ABCA1)), leukocyte recruitment (C-C motif chemokine ligand 2 (CCL2), osteopontin (OPN), interleukin (IL)-6), and leukocyte rolling, extravasation and adhesion (vascular cell adhesion molecule (VCAM)-1, E-selectin (SELE)) [16]

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It all comes down to one tiny villain: acetaldehyde