ArticleCell death discovery2024
Peds1 deficiency in zebrafish results in myeloid cell apoptosis and exacerbated inflammation.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed.
- Origin of eukaryotic plasmalogen biosynthesis by horizontal gene transfer from myxobacteria.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Zebrafish as a translational platform for investigating multi-organ pharmacological interactions of traditional Chinese medicine.Frontiers in pharmacology · 2026Review
- Lipidomics of polarized macrophages in the human adipose tissue.Scientific reports · 2025Article
- Programmed cell death pathways coordinate neutrophil and macrophage clearance in zebrafish and are differentially exploited by Salmonella Typhimurium.Cell death & disease · 2025Article
- LncPEDS1-AS promotes UTUC resistance to lipid peroxidation by regulating PEDS1 expression via DDX23.Cell death & disease · 2025Article
- Alterations in ether lipid metabolism in obesity revealed by systems genomics of multi-omics datasets.PLoS biology · 2025Article
- Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Plasmalogens are glycerophospholipids with a vinyl ether bond that confers unique properties. Recent identification of the gene encoding PEDS1, the desaturase generating the vinyl ether bond, enables evaluation of the role of plasmalogens in health and disease. Here, we report that Peds1-deficient zebrafish larvae display delayed development, increased basal inflammation, normal hematopoietic stem and progenitor cell emergence, and cell-autonomous myeloid cell apoptosis. In a sterile acute inflammation model, Peds1-deficient larvae exhibited impaired inflammation resolution and tissue regeneration, increased interleukin-1β and NF-κB expression, and elevated ROS levels at the wound site. Abnormal immune cell recruitment, neutrophil persistence, and fewer but predominantly pro-inflammatory macrophages were observed. Chronic skin inflammation worsened in Peds1-deficient larvae but was mitigated by exogenous plasmalogen, which also alleviated hyper-susceptibility to bacterial infection, as did pharmacological inhibition of caspase-3 and colony-stimulating factor 3-induced myelopoiesis. Overall, our results highlight an important role for plasmalogens in myeloid cell biology and inflammation.
Identifiers
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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.