ArticleThe EMBO journal2019
Prdx4 limits caspase-1 activation and restricts inflammasome-mediated signaling by extracellular vesicles.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Correlation of high PRDX4 expression with poor prognosis in patients with ESCA: Bioinformatics andMolecular and clinical oncology · 2026Article
- Targeting eEF1A1 With Baicalein to Block eEF1A1/Prdx4 Interaction for Treating Sepsis-Mediated Lung Injury.Exploration (Beijing, China) · 2026Article
- Evolution of botulinum neurotoxin serotype X proteases to induce inflammatory cell death in cancer cells.Nature biotechnology · 2026Article
- Peroxiredoxin 4 as a switch regulating PTEN/AKT axis in alveolar macrophages activation.Signal transduction and targeted therapy · 2025Article
- Dynamic changes of extracellular vesicles during zebrafish organogenesis.Cell communication and signaling : CCS · 2025Article
- Integrative MultiOmics and Machine Learning Reveal Peroxiredoxin 4 as a Critical Hub Governing Mitochondrial Dysfunction and B Cell Differentiation in Periodontitis.Clinical, cosmetic and investigational dentistry · 2025Article
- The oxidative modification of transcription factor FOXM1 by Peroxiredoxin1 facilitates DNA damage repair and cancer progression.American journal of cancer research · 2025Article
- Identification and Validation of Feature Genes Related to Mitochondrial Dysfunction and Oxidative Stress in Ulcerative Colitis.Journal of inflammation research · 2025Article
- Pathogenic and therapeutic roles of extracellular vesicles in sepsis.Frontiers in immunology · 2025Review
- Zinc finger protein 593 promotes breast cancer development by ensuring DNA damage repair and cell-cycle progression.iScience · 2024Article
- Dynamic changes in extracellular vesicle-associated miRNAs elicited by ultrasound in inflammatory bowel disease patients.Scientific reports · 2024Article
- Revealing Prdx4 as a potential diagnostic and therapeutic target for acute pancreatitis based on machine learning analysis.BMC medical genomics · 2024Article
- Validation of the interaction between PRDX4 and TXNDC5 in gastric cancer and the significance of theTranslational cancer research · 2024Article
- Screening of pathologically significant diagnostic biomarkers in tears of thyroid eye disease based on bioinformatic analysis and machine learning.Frontiers in cell and developmental biology · 2024Article
- Peroxiredoxin-4 and Dopamine D5 Receptor Interact to Reduce Oxidative Stress and Inflammation in the Kidney.Antioxidants & redox signaling · 2023Article
- Redox proteomics combined with proximity labeling enables monitoring of localized cysteine oxidation in cells.Cell chemical biology · 2023Article
- Remarkable sex-specific differences at single-cell resolution in neonatal hyperoxic lung injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Essential Roles of Peroxiredoxin IV in Inflammation and Cancer.Molecules (Basel, Switzerland) · 2022Review
- Article
- The Role of Peroxiredoxins in the Regulation of Sepsis.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 4 countries.
Funding
Abstract
Inflammasomes are cytosolic protein complexes, which orchestrate the maturation of active IL-1β by proteolytic cleavage via caspase-1. Although many principles of inflammasome activation have been described, mechanisms that limit inflammasome-dependent immune responses remain poorly defined. Here, we show that the thiol-specific peroxidase peroxiredoxin-4 (Prdx4) directly regulates IL-1β generation by interfering with caspase-1 activity. We demonstrate that caspase-1 and Prdx4 form a redox-sensitive regulatory complex via caspase-1 cysteine 397 that leads to caspase-1 sequestration and inactivation. Mice lacking Prdx4 show an increased susceptibility to LPS-induced septic shock. This effect was phenocopied in mice carrying a conditional deletion of Prdx4 in the myeloid lineage (Prdx4-ΔLysMCre). Strikingly, we demonstrate that Prdx4 co-localizes with inflammasome components in extracellular vesicles (EVs) from inflammasome-activated macrophages. Purified EVs are able to transmit a robust IL-1β-dependent inflammatory response in vitro and also in recipient mice in vivo. Loss of Prdx4 boosts the pro-inflammatory potential of EVs. These findings identify Prdx4 as a critical regulator of inflammasome activity and provide new insights into remote cell-to-cell communication function of inflammasomes via macrophage-derived EVs.
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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.