Evidence map›Paper›PMID 37066876›Full record

ArticleThe Journal of clinical investigation2023

Mycobacterium tuberculosis hijacks host TRIM21- and NCOA4-dependent ferritinophagy to enhance intracellular growth.

Youchao Dai, Chuanzhi Zhu, Wei Xiao, Kaisong Huang, Xin Wang, Chenyan Shi, Dachuan Lin, Huihua Zhang, Xiaoqian Liu, Bin Peng and 7 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  7. Article
  8. Review
  9. Review
  10. Article
  11. Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  15. Review
  16. Article
  17. The Ubiquitination ofBiology · 2025
    Article
  18. Article
  19. Review
  20. Autophagy · 2025
    Article
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

17 authors at 10 institutions in 4 countries.

Youchao DaiGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Chuanzhi ZhuLaboratory of Molecular Biology, Beijing Key Laboratory for Drug Resistance Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, China.
Wei XiaoGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Kaisong HuangZhuhai Center for Disease Control and Prevention, Zhuhai, China.
Xin WangFirst Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Chenyan ShiGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Dachuan LinGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Huihua ZhangGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Xiaoqian LiuIntegrated Chinese and Western Medicine Postdoctoral Research Station, Jinan University, Guangzhou, China.
Bin PengGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Yi GaoSchool of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, China.
Cui Hua LiuCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Beijing, China.
Baoxue GeShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Stefan He KaufmannMax Planck Institute for Infection Biology, Berlin, Germany.
Carl G FengImmunology and Host Defense Group, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia.
Xinchun ChenGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Yi CaiGuangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China.
Shenzhen University · CNShenzhen University Health Science Center · CNCapital Medical University · CNChinese Academy of Sciences · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNInstitute for Advanced Study · USJinan University · CNTongji University · CNUNSW Sydney · AUZhuhai People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferritin, a key regulator of iron homeostasis in macrophages, has been reported to confer host defenses against Mycobacterium tuberculosis (Mtb) infection. Nuclear receptor coactivator 4 (NCOA4) was recently identified as a cargo receptor in ferritin degradation. Here, we show that Mtb infection enhanced NCOA4-mediated ferritin degradation in macrophages, which in turn increased the bioavailability of iron to intracellular Mtb and therefore promoted bacterial growth. Of clinical relevance, the upregulation of FTH1 in macrophages was associated with tuberculosis (TB) disease progression in humans. Mechanistically, Mtb infection enhanced NCOA4-mediated ferritin degradation through p38/AKT1- and TRIM21-mediated proteasomal degradation of HERC2, an E3 ligase of NCOA4. Finally, we confirmed that NCOA4 deficiency in myeloid cells expedites the clearance of Mtb infection in a murine model. Together, our findings revealed a strategy by which Mtb hijacks host ferritin metabolism for its own intracellular survival. Therefore, this represents a potential target for host-directed therapy against tuberculosis.

Indexed as

Mycobacterium tuberculosisTuberculosisAnimalsAutophagyFerritinsHumansIronMiceNuclear Receptor CoactivatorsTranscription FactorsFerritinsIronNCOA4 protein, humanNcoA4 protein, mouseNuclear Receptor CoactivatorsTranscription FactorsBacterial infectionsImmunologyInfectious diseaseInnate immunity

Identifiers

PMID37066876
PMCPMC10104892
OpenAlexW4365998968

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.