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Autophagic Punctum

WIP-ing out atherosclerosis with autophagy

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Pages 1545-1547 | Received 03 Jul 2012, Accepted 06 Jul 2012, Published online: 16 Aug 2012

Figures & data

Figure 1. A role for PPM1D in atherosclerosis. In early atherosclerosis, macrophages take up oxLDL, process it and deposit cholesterol esters in the form of cytoplamic LDs as shown in (A). If autophagy is activated through the PPM1D-ATM-MTOR pathway, LDs are fused with autophagosome and subsequently with lysosomes, free cholesterol is produced, and it is subsequently effluxed from the cell. In advanced stages of atherosclerosis (B), cholesterol is trapped in lysosomes of foam cells. The prediction is that the PPM1D/ATM‐dependent inhibition of the MTOR pathway at this stage could also lead to activation of autophagy-dependent cholesterol efflux as well as LC3-associated clearance of dead cells.

Figure 1. A role for PPM1D in atherosclerosis. In early atherosclerosis, macrophages take up oxLDL, process it and deposit cholesterol esters in the form of cytoplamic LDs as shown in (A). If autophagy is activated through the PPM1D-ATM-MTOR pathway, LDs are fused with autophagosome and subsequently with lysosomes, free cholesterol is produced, and it is subsequently effluxed from the cell. In advanced stages of atherosclerosis (B), cholesterol is trapped in lysosomes of foam cells. The prediction is that the PPM1D/ATM‐dependent inhibition of the MTOR pathway at this stage could also lead to activation of autophagy-dependent cholesterol efflux as well as LC3-associated clearance of dead cells.

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