ArticleJournal of advanced research2026
The immune regulation and signaling transduction of FAM134B-mediated endoplasmic reticulum-phagy in ferroptosis of dendritic cells after sepsis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
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Who cites it
3 citing papers in PubMed.
- Ferroptosis in T cells: mechanisms, biology and translational opportunities.Nature reviews. Immunology · 2026Review
- The emerging role of ERphagy/reticulophagy in pathogen invasion.Autophagy · 2026Article
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionFam134B-mediated endoplasmic reticulum (ER)-phagy is one of the key mechanisms for maintaining functional homeostasis of ER and cell survival. In fact, Fam134B-mediated ER-phagy has been proved to exert a double-edged sword in response to inflammatory and oxidative stress, which is evidenced by the recovery effect on an appropriate organellar autophagy whereas the activation of cell death in excessive condition. However, its potential role and significance in regulating the immunoreaction within the framework of sepsis and its associated mechanisms remain to be elucidated.
objectivesThe present research aimed to explore the effects of FAM134B on mediating ER-phagy in DCs after sepsis.
methodsBy use of DCs from FAM134B
resultsThe upregulation of FAM134B upon septic challenge could exert a protective impact on ferroptosis and immune function of dendritic cells (DCs). FAM134B -mediated ER-phagy was activated in DCs stimulated by LPS (1 μg/ml) at the peak time of 12 h, which presented a parallel impact on DCs. DCs in genetic knockout mice for FAM134B (FAM134B
conclusionThis study demonstrated the intrinsic connection between FAM134B -mediated ER-phagy, ferroptosis, as well as sepsis-induced immune dysfunction, which might provide new targeted strategies for immune modulation in septic complications.
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