Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed-forward loop between LXR and autophagy.
Peter Saliba-GustafssonMatteo PedrelliK GertowO WerngrenV JanasS PourteymourD BaldassarreE TremoliF VegliaR RauramaaA J SmitP GiralSudhir KurlM PirroU de FaireS E HumphriesA Hamstennull nullI GonçalvesM Orho-MelanderA Franco-CerecedaJan BorénPer ErikssonJ MagnéPaolo PariniEwa EhrenborgPublished in: Journal of internal medicine (2019)
For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis.