ArticleEmerging microbes & infections2025
Monkeypox virus induces ferroptosis to facilitate viral replication and promotes inflammatory responses.
Article in Emerging microbes & infections, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Ferroptosis: significance to zoonotic diseases and therapeutic prospects.Emerging microbes & infections · 2026Review
- Novel Duck Orthoreovirus Induces Ferroptosis in HD11 Cells by Hijacking Cellular Iron Metabolism and Promoting Iron Accumulation.Transboundary and emerging diseases · 2026Article
- Ciclopirox suppresses poxvirus replication by targeting iron metabolism.Antiviral research · 2025Article
Corrections and comments
- Retracted
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is an iron-dependent form of programmed cell death, which is characterized by iron overload and accumulation of lipid peroxidation. As a newly identified type of cell death, its involvement in poxvirus infection and pathogenesis remains unclear. Since MPXV shares biological and pathogenic similarities with other poxviruses, such as vaccinia virus (VACV), we used VACV-infected cell and mouse models to demonstrate that VACV infection induces ferroptosis both in vitro and in vivo. Inhibition of ferroptosis significantly reduce virus replication and alleviates the inflammatory response. Additionally, we observed that VACV infection upregulates prostaglandin-endoperoxide synthase 2 (PTGS2), which contributes to virus-triggered ferroptosis and inflammation. This study identifies a novel form of cell death triggered by poxvirus infection, shedding light on host-pathogen interactions and offering a potential therapeutic target for MPXV and other
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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.