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Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux
Lack of Peroxiredoxin 1 lowers cholesterol removal by disrupting fat cleanup in immune cells
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Abstract
PRDX1 expression is crucial for maintaining lipophagic flux in macrophages.
- PRDX1 is more highly expressed in monocytes and macrophages compared to other antioxidant enzymes.
- Deficiency of Prdx1 leads to excessive oxidative stress and impaired autophagic flux in macrophages.
- Prdx1-deficient macrophages exhibit higher intracellular cholesterol mass and lower than wild type.
- Impaired lipophagic cholesterol hydrolysis due to oxidative stress inhibits free cholesterol formation and reduces NR1H3 activity.
- Restoration of lipophagic flux and cholesterol efflux in deficient macrophages can be achieved with PRDX-mimics ebselen and gliotoxin.
- Bone marrow transplantation from prdx1-deficient mice into apoemice results in increased plaque formation.
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Key numbers
significantly lower
Decrease in
was significantly reduced in macrophages from PRDX1-deficient mice.
increased
Increased Plaque Formation
Bone marrow from PRDX1-deficient mice led to more plaque formation in recipients.