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Hepatic lipid metabolism is profoundly affected by cigarette smoke; which likely contributes to the atherogenic plasma lipid profile observed in cigarette smokers. There is, however, a paucity of data on the identification of molecular networks and mechanisms responsible for the reduction of cardiovascular risk in former smokers compared to the risk of current smokers. Using ApoE-/- mice, an experimental model exhibiting a high atherogenic rate that leads to rapid development of vascular lesions, we investigated the effects of discontinuing smoke exposure on both hepatic lipid and transcriptome profiles. Livers from ApoE-/- mice exposed to: (i) mainstream smoke of the reference research cigarette 3R4F for six months (CS), (ii) fresh air for six months (sham exposed), or (iii) CS for three months followed by fresh air for three months (cessation), were extracted and their lipid composition analyzed on six different mass spectrometry platforms.
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