ArticleDevelopmental cell2025
Paraoxonase-like APMAP maintains endoplasmic-reticulum-associated lipid and lipoprotein homeostasis.
Article in Developmental cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Coenzyme Q10 protects against 6 GHz electromagnetic field-induced liver injury via suppression of inflammatory responses associated with NF-κB/p65 immunoreactivity and endoplasmic reticulum stress.Scientific reports · 2026Article
- 15-LOX-catalytic bias towards ether-(alkenyl)-ETE-PEs oxidation bestows selectivity of PRO-ferroptotic cell death signaling.Nature communications · 2026Article
- Transcriptomics and 4D-DIA proteomic analysis reveal differences in meat quality between Sichuan white rabbits and New Zealand white rabbits.Food chemistry. Molecular sciences · 2026Article
- Organelle-specific regulation of ferroptosis.Biology direct · 2026Review
- Current and Emerging Issues in Familial Hypobetalipoproteinemia-related Steatotic Liver Diseases.Journal of clinical and translational hepatology · 2025Review
- The plasma proteome reveals markers of recent and repeated stress in free-ranging seals.Conservation physiology · 2024Article
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Abstract
Oxidative stress perturbs lipid homeostasis and contributes to metabolic diseases. Though ignored when compared with mitochondrial oxidation, the endoplasmic reticulum (ER) generates reactive oxygen species requiring antioxidant quality control. Using multi-organismal profiling featuring Drosophila, zebrafish, and mammalian hepatocytes, here we characterize the paraoxonase-like C20orf3/adipocyte plasma-membrane-associated protein (APMAP) as an ER-localized antioxidant that suppresses ER lipid oxidation to safeguard ER function. APMAP-depleted cells exhibit defective ER morphology, ER stress, and lipid peroxidation dependent on ER-oxidoreductase 1α (ERO1A), as well as sensitivity to ferroptosis and defects in ApoB-lipoprotein homeostasis. Similarly, organismal APMAP depletion in Drosophila and zebrafish perturbs ApoB-lipoprotein homeostasis. Strikingly, APMAP loss is rescued with chemical antioxidant N-acetyl-cysteine (NAC). Lipidomics identifies that APMAP loss elevates phospholipid peroxidation and boosts ceramides-signatures of lipid stress. Collectively, we propose that APMAP is an ER-localized antioxidant that promotes lipid and lipoprotein homeostasis in the ER network.
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