ArticleAutophagy2018
Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux.
Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
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- A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques.Bioactive materials · 2026Article
- The transcription factor HHEX maintains glucocorticoid levels and protects adrenals from androgen-induced lipid depletion.Nature communications · 2026Article
- RNASEH2C enhances TRAF3IP1 to degrade RAI14 in lysosomes thus hindering macrophage antigen presentation and advancing liver cancer.Cell death & disease · 2025Article
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- PRDX1 promotes testosterone synthesis and attenuates aging via redox regulation of ATG4B to modulate lipophagy.Nature communications · 2025Article
- A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Macrophages and autophagy: partners in crime.The FEBS journal · 2025Review
- Circulating metabolites of Borneolum syntheticum (Bingpian) ameliorate atherosclerosis in ApoEActa pharmacologica Sinica · 2025Article
- Multi-omics dissection of fatty acid metabolism heterogeneity identifies PRDX1 as a prognostic marker in bladder cancer.Frontiers in immunology · 2025Article
- Integrative multi-omics analysis of IFNγ-induced macrophages and atherosclerotic plaques reveals macrophage-dependent STAT1-driven transcription in atherosclerosis.Frontiers in immunology · 2025Article
- Integrated multi-omic profiling reveals macrophage-driven prognostic signatures in clear cell renal cell carcinoma through machine learning optimization.Frontiers in immunology · 2025Article
- Article
- The senescent marker p16INK4a enhances macrophage foam cells formation.Molecular biology reports · 2024Article
- Leveraging gene correlations in single cell transcriptomic data.BMC bioinformatics · 2024Article
- Huayu Qutan Recipe promotes lipophagy and cholesterol efflux through the mTORC1/TFEB/ABCA1-SCARB1 signal axis.Journal of cellular and molecular medicine · 2024Article
- Leveraging gene correlations in single cell transcriptomic data.bioRxiv : the preprint server for biology · 2023Article
- Unbalanced Redox With Autophagy in Cardiovascular Disease.Journal of lipid and atherosclerosis · 2023Review
- Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway.Iranian journal of basic medical sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 9 institutions in 5 countries.
Funding
Abstract
Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous antioxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the antioxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other antioxidant enzymes in monocytes and macrophages. We determined that Prdx1 deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages. Prdx1-deficient macrophages had higher intracellular cholesterol mass and lower cholesterol efflux compared with wild type. This perturbation in cholesterol homeostasis was due to impaired lipophagic cholesterol hydrolysis caused by excessive oxidative stress, resulting in the inhibition of free cholesterol formation and the reduction of NR1H3 (nuclear receptor subfamily 1, group H, member 3) activity. Notably, impairment of both lipophagic flux and cholesterol efflux was restored by the 2-Cys PRDX-mimics ebselen and gliotoxin. Consistent with this observation, apoe
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.