Evidence map›Paper›PMID 37777065›Full record

ArticleJournal of advanced research2024

IFP35 aggravates Staphylococcus aureus infection by promoting Nrf2-regulated ferroptosis.

Min Dai, Wei Ouyang, Yangle Yu, Tao Wang, Yanling Wang, Mengyuan Cen, Liping Yang, Yu Han, Yushi Yao, Feng Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Emerging microbes & infections · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Min DaiDepartment of Infectious Diseases, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Wei OuyangDepartment of Infectious Diseases, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Yangle YuInstitute of Immunology, Zhejiang University School of Medicine, 310009, China.
Tao WangInstitute of Immunology, Zhejiang University School of Medicine, 310009, China.
Yanling WangInstitute of Immunology, Zhejiang University School of Medicine, 310009, China.
Mengyuan CenDepartment of Respiratory Medicine, Ningbo First Hospital, Ningbo 315010, China.
Liping YangDepartment of Gastroenterology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, China.
Yu HanDepartment of Infectious Diseases, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Yushi YaoInstitute of Immunology, Zhejiang University School of Medicine, 310009, China.
Feng XuDepartment of Infectious Diseases, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China; Research Center for Life Science and Human Health, Binjiang Institute of Zhejiang University, Hangzhou 310053, China. Electronic address: xufeng99@zju.edu.cn.
Institute of Immunology · HRSecond Affiliated Hospital of Zhejiang University · CNNingbo First Hospital · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSerious Staphylococcus aureus (SA) infection is one of the most life-threatening diseases. Interferon-induced protein 35 (IFP35) is a pleiotropic factor that participates in multiple biological functions, however, its biological role in SA infection is not fully understood. Ferroptosis is a new type of regulated cell death driven by the accretion of free iron and toxic lipid peroxides and plays critical roles in tissue damage. Whether ferroptosis is involved in SA-induced immunopathology and its regulatory mechanisms remain unknown.

objectivesWe aimed to determine the role and underlying mechanisms of IFP35 in SA-induced lung infections.

methodsSA infection models were established using wild-type (WT) and IFP35 knockout (Ifp35

resultsWe found that IFP35 levels increased in the macrophages and lung tissue of SA-infected mice. IFP35 deficiency protected against SA-induced lung damage in mice. Moreover, ferroptosis occurred and contributed to lung injury after SA infection, which was ameliorated by IFP35 deficiency. Mechanically, IFP35 facilitated the ubiquitination and degradation of nuclear factor E2-related factor 2 (Nrf2), aggravating SA-induced ferroptosis and lung injury.

conclusionsOur data demonstrate that IFP35 promotes ferroptosis by facilitating the ubiquitination and degradation of Nrf2 to exacerbate SA infection. Targeting IFP35 may be a promising approach for treating infectious diseases caused by SA.

Indexed as

FerroptosisNF-E2-Related Factor 2Staphylococcal InfectionsStaphylococcus aureusAnimalsDisease Models, AnimalHumansLungMacrophagesMiceMice, Inbred C57BLMice, KnockoutNfe2l2 protein, mouseNF-E2-Related Factor 2FerroptosisIFP35NRF2Staphylococcus aureusUbiquitination

Identifiers

PMID37777065
PMCPMC11331171
OpenAlexW4387122214

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.